THE
ROLE OF THE BURSA OF FABRICIUS
AND HIGHLY DILUTE BURSIN
IN IMMUNONEUROENDOCRINE INTERACTIONS
IN THE CHICKEN
Biological
effects of highly dilute bursin
B.J. YOUBICIER-SIMO*, F. BOUDARD*,
M. GUELATTI**, M. MEKAOUCHE**, J.D. BAYLÉ**,
AND M. BASTIDE*
* Laboratoire
d'Immunologie & Parasitologie
Faculté de Pharmacie,
Université de Montpellier-1
15 Av. Ch. Flahault,
34060, Montpellier cedex 1, France
** Laboratoire
de Physiologie Générale
Faculté des
Sciences, Université de Montpellier-2
Pl. E. Bataillon,
34090 Montpellier cedex 5 (France)
1
- Introduction
2 - Material and Methods
3 - Results
4 - Discussion
5 - References
A huge set of data, pertaining to Mammals namely, supports
the existence of two-way communication between the immune and neuroendocrine
systems. For example, glucocorticoids released by the adrenals are immunodepressive;
in turn, immune products act at different levels of the hypothalamo-pituitary-adrenal
axis (HPA) (for review see Lilly and Gann, 1992). Also, the chief pineal hormone
melatonin (MLT) is immunostimulatory (Maestroni et al., 1989) whereas interferon-g stimulates the release of MLT by cultured pineal glands (Withyachumnarkul
et al., 1990). The concept that products of the immune system act on the neuroendocrine
system was suggested by Besedovsky and Sorkin (1977), based on their observation
that in rats, serum corticosterone (CORT) increases during the course of immune
response. However, in Mammals, most studies working out immunoneuroendocrine
interferences deal with the T immune component mainly, therefore neglecting
the involvement of the B lymphoid compartment, because the latter is rather
anatomically diffuse. Therefore, it appears experimentally difficult to identify
specific B immune signal (s) endowed with neuroendocrine competence.
Aves
possess a species specific and anatomically distinct organ termed the bursa
of Fabricius (Toivanen et al., 1981).
The latter is a diverticulum of the hindgut and it is also the primary site
for B-cell differentiation (Toivanen et
al., 1981). The bursa anlage arises by the 5 th day of embryonic development
as a swelling of the cloacal plate and it is invaded by B stem cells between
the 8 th and 14 th day of embryonic life (Le Douarin et al., 1975; Houssaint et al.,
1976; Lassila et al., 1978). In
the bursa follicles, the B precursor cells differentiate into mature lymphocytes
which seed to the periphery by the end of the embryonic phase (Le Douarin
et al., 1975; Weill and Reynaud,
1987). Early removal of the bursa anlage leads to permanent B-deficient chickens
(Fitzsimmons et al., 1973; Jankovic
et al., 1977; Granfors et
al., 1982; Jalkanen et al., 1983). This surgical procedure
provides a biological preparation suitable for the study of possible involvement
of the B immune component in immunoneuroendocrine crosstalks. The function
of the bursa of Fabricius is mediated by cellular and soluble factors that
have been identified as integral parts of the bursa microenvironment (Heller
and Friedman, 1979; Glick, 1984ab; Kuznik et al., 1988). One of these factors is a low-molecular weight inducing
agent termed bursopoietin that has been extracted from the chicken bursa (Brand
et al., 1976). This agent has been
isolated, purified and termed bursin (Lys-His-Gly-NH2) by the US
team of Goldstein (Audhya et al.,
1986). Bursin has been immunohistochemically identified in the bursal epithelium
(Viamontes et al., 1989), as well
as in avian and bovine bone marrow and in the intrahepatic bile ducts of bovidæ
(Audhya et al., 1990). A tetradecapeptide
precursor named probursin and containing the sequence of bursin, tuftsin and
the active site of somatostatin has also been discovered (Audhya et
al., 1991). Bursin induces B cells from their avian and mouse precursors
in vitro (Goldstein et al.,
1977; Audhya et al., 1986; Lassila
et al., 1989). However, it is still unclear
whether the neuroendocrine function of the bursa of Fabricius also operates
through bursin-dependent mechanisms.
The present study was an attempt to disclose the possible
involvement of the B immune component in immunoneuroendocrine interactions,
using permanent B-deficient chickens (bursectomized chickens). This aim was
achieved by testing:
1.
the ability of bursectomized chickens to respond hormonally and immunologically
to various environmental agents (ether vapour, antigen, photoperiod). The
following parameters were assessed:
-
the pituitary (corticotrophin: ACTH) and adrenal (corticosterone: CORT) responses
to ether vapour exposure,
-
the specific antibody (IgM, IgG), as well as the pituitary-adrenal (ACTH,
CORT) and pineal (melatonin: MLT) responses to immunization against porcine
thyroglobulin (Tg),
-
the nature of the endocrine responses displayed by porcine Tg-sensitized chickens,
-
the circadian rhythms of both pituitary-adrenal (ACTH, CORT) and pineal (MLT,
N-acetyltransferase: NAT, hydroxyindole-o-methyltransferase: HIOMT) activities.
2. the effectiveness of the bursa-derived signal
(bursin) in reversing the effects of bursectomy, by means of in ovo administration of different amounts
of bursin (100 µg, 100 pg (5CH), 100 fg ( 7CH), 5 x 10-27 g (a pool of 15CH to 20 CH dilutions) to bursectomized
embryos.
2.1. INCUBATION
OF EGGS AND CHICKS MANAGEMENT
Eggs from New Hampshire strain were purchased from Couvoir
des Cévennes (Ledenon 30, France) and incubated in a Maino Ladi France incubator
(38 ± 1° C, 45-50% humidity, permanent darkness). An incorporated electric
fan allowed homogeneity of the temperature and air inside the incubator. The
eggs were permanently turned on automatically rotating drawers with 45° maximal
inclination, so as to avoid sweating of the eggs opened during surgical bursectomy.
Newly-hatched
chicks were housed under controlled photoperiod [12 h light (0700-1900), 12
h dark] and the environmental temperature was progressively reduced 1° C per
day from 38° C to 22° C. Feed and water were available ad-libitum.
2. 2. SURGICAL METHODS
2. 2. 1. Embryonic bursectomy
The removal of the bursa anlage was performed at 80 h
of incubation (4 th day of embryonic life) according to Fitzsimmons et al. (1973). The surgical operation was
carried out under aseptic conditions. Briefly, the embryo was localized into
the egg by candling and the shell was opened above it using fine forceps.
Then a small slit was made in the chorion and amnios at the level of the caudal
bud. A sterilized fine loop was passed over the caudal bud and tightened posterior
to the leg buds, caudally to the cloacal membrane. The tail was cut off posterior
to the nod using microsurgical scissors and the free fragment was discarded.
The lips of the chorion and amnios were closed with forceps and the shell
opening was overlaid with parafilm M and sealed with paraffin.
2. 2. 2. Removal
of the pineal glands and eyes
The chickens were sacrificed by decapitation and the
skull was opened dorsally between the cerebral hemispheres and the cerebellum.
The meninges were slit above the pineal gland along the line of suture. The
lips of the opening were drawn aside by means of slender forceps. The pineal
body gripped by its stalk, withdrawn from the skull, immediately frozen in
liquid nitrogen and stored at -80° C until assayed for the pineal enzymatic
activities (NAT, HIOMT). The eyes from each bird were dissected out, wrapped
individually in aluminium foil, immediately frozen in liquid nitrogen and
stored at -20° C until time of assay. Then the retinae were isolated by the
procedure described by Hamm and Menaker (1980).
2. 3. TRIPEPTIDES AND IN OVO TREATMENT
Bursin (Lys-His-Gly-NH2) was synthesized de novo
by fragment peptide coupling (Le Nguyen, 1987). The control tripeptide
(Trp-Leu-Leu-NH2) was a gift from Dr. Martinez, University of Montpellier,
France). The injected solutions were prepared by sequential centesimal dilution
steps including potent vertical stirring between two successive steps. On
the 6 th and 9 th day of incubation, the embryos were treated in
ovo by single administration of 100 µl of solution each day in the yolk
sack , as follows: sham-bursectomized embryos (N) were given 100 µl of saline
(N+S). The surgical treatment group (Bx) could receive either 100 µl of saline
(Bx+S) or 100 µl of saline containing 5 CH of the control peptide (Bx+Pf)
or 100 µl of saline containing different doses of bursin: 100 µg (Bx+Bµ)
or 5 CH (Bx+Bp) or 7 CH (Bx+Bf) or a 15-20 CH pool (Bx+B-27).
2. 4. EXPERIMENTAL GROUPS
The birds were distributed as follows:
N: Sham-bursectomized (the surgical handling
was limited to opening and closing the chorion and amnios in 80 h old embryos),
N+S: sham-bursectomized birds injected
in the yolk sack by single administration of 100 µl of saline on the 6 th
and 9 th day of embryonic life,
Bx: chickens embryonically bursectomized
at 80 h of incubation,
Bx+B: chickens embryonically bursectomized
at 80h of incubation and supplemented on the 6th and 9th day of embryonic
development by in ovo administration
of 100 µl of saline containing different amounts of bursin: 100 µg (Bx+Bµ) or 5 CH (Bx+Bp) or 7 CH (Bx+Bf) or the 15-20 CH pool
(Bx+B-27),
Bx+Pf: chickens embryonically
bursectomized at 80 h of incubation and receiving 100 µl of saline containing
5 CH of the control tripeptide (Trp-Leu-Leu-NH2) on the 6 th and
9 th day of embryonic development.
2. 5. ANTIGENS
Porcine Tg or keyhole limpet hemocyanin (KLH) purchased
from Sigma was injected subcutaneously. The dose of immunogen to be injected
was determined in a preliminary experiment (data not shown). Chickens received
three doses of 125 µg/100 g B.W. (750
µg/ml of saline) mixed (v/v) with complete (first immunization) or incomplete
(second and third immunizations) Freund adjuvant.
2. 6. EXPERIMENTAL DESIGN
Four experimental protocols including a total of 10 experiments
have been carried out during six years.
2. 6. 1. First
protocol
Experiment 1. Five chicken samples were used: N (4), Bx (4), Bx+Bµ
(4), Bx+Bp (4), Bx+Bf (3). In brakets is the number
of animals. Eight week-old chickens were placed in an ether vapour saturated
box for 1min between 0900 and 1000. Blood samples were withdrawn from the
brachial vein 7 and 14 min after ether vapour application, and assayed for
plasma ACTH and CORT respectively.
2. 6. 2. Second
protocol
This protocol was designed to measure the hormonal and
specific humoral immune responses to antigen challenge. Four expriments were
performed (experiments 2, 3, 4, 5). In experiments 2, 3 and 4, young chickens
were repeatedly immunized by injecting porcine Tg at 21, 30 and 39 days of
age. Blood samples were withdrawn from the brachial vein, within 30 s, between
0900 and 1000, the day before immunization (d20) and at 9 day intervals after
the first (d29), the second (d38) and the third (d47) antigen challenge. All
the sera were blinded before hormones and antibody evaluation. The specificity
of anti-Tg antibodies was also determined.
Experiment 2. The following groups of animals were used: N (8), Bx
(7), Bx+Bµ (6), Bx+Bp (6) and Bx+Bf (7).
The plasma levels of ACTH, CORT and MLT, as well as the serum titres of specific
anti-Tg antibodies (IgM, IgG) were measured.
Experiment 3. It was carried out with 4 groups of chickens: N (8),
Bx+S (6), Bx+Bf (9), Bx+B-27 (7). The plasma levels of CORT, as well as the serum
titres of anti-Tg IgG antibodies were determined.
Experiment 4. Seven chicken samples were studied: N (7), N+S (6),
Bx (11), Bx+S (7), Bx+Pf (4), Bx+Bf (7), Bx+B-27 (8). The
following parameters were assessed: the plasma levels of ACTH, CORT and MLT,
as well as the serum titres of specific anti-Tg IgG.
Experiment 5. This experiment was designed to determine if the hormonal
responses of bursa-intact chickens sensitized to porcine Tg derived from metabolic
reactions involving Tg or if these answers were linked to the immunization
phenomenon. Tg is the endogenous prohormone of thyroid hormones which themselves
modulate the pituitary-adrenal activity during the course of immune response
(Besedovsky et al., 1975; Trout
et al., 1988). Keyhole limpet hemocyanin
(KLH) is a T-dependent antigen without any pharmacological activity. To attempt
disclosing the nature of the hormonal response to porcine Tg, 17 bursa-intact
chickens immunized against porcine Tg were compared with their KLH-sensitized
counterparts (18 chickens) for CORT, MLT and IgG responses. The chickens were
immunized at 21, 30 and 36 days of age by subcutaneous inoculation of either
porcine Tg or KLH. Blood samples were collected between 0900 and 1000 at the
age of 20 (d20), 29 (d29), 35 (d35) and 38 (d38). Then the plasma levels of
CORT and MLT, as well as the serum titers of anti-Tg or anti-KLH antibodies
(IgG) were measured.
2. 6. 3. Third
protocol
Twelve week-old chickens raised since hatching under
a 12L00700-1900-12D alternating light-dark regime underwent four
experiments (experiments 6, 7, 8, 9).
Experiment 6.
In this preliminary experiment,
bursa-intact chickens (N, 13) were decapitated and their circulating, ocular
and pineal MLT contents were measured between 1200 and 1300 and between 0000
and 0100 (under red light).
Experiment 7. Five samples were studied: N (9), Bx (3), Bx+Bµ
(3), Bx+Bp (3) and Bx+Bf (9). The chickens were bled
at two-point time, between 1200 and 1300 and between 2000 and 2100 (under
red light) to assess plasma ACTH and CORT levels. MLT levels were measured
in blood samples collected between 1200 and 1300 and between 0000 and 0100
(under red light).All the sera were blinded before hormones evaluation.
Experiment 8. Blood samples were withdrawn from the N (7), Bx (5),
Bx+Bf (4) and Bx+B-27 (4) groups between 1200 and 1300
and between 0000 and 0100 (under red light) to assess the plasma levels of
MLT. After blood sampling, the animals were immediately sacrificed by decapitation
and their pineal tissues assayed for NAT and HIOMT activities.
Experiment 9. Blood samples were collected from the brachial vein
at 4 h intervals around the clock (1000, 1400, 1800, 2200, 0200, 0600) to
measure the plasma levels of ACTH, CORT and MLT. The chicken samples used
were as follows: N (13), N+S (6), Bx (12), Bx+S (7), Bx+Pf (4),
Bx+Bf (7), Bx+B-27 (7). All the sera
were blinded before hormones evaluation.
2. 6. 4. Fourth
protocol
Experiment 10.
This experiment was aimed at checking whether a succussed highly dilute solution
of bursin was structurally different from the same dilution unsuccussed. To
answer this question, we decided to measure the concentration of labelled
bursin in serial dilutions of this compound. Since labelled
bursin was not available on the market place, we used 3H-Thymidine.
3H-Thymidine (cpm) was measured in different concentrations of succussed
thymidine solutions ranging from 10-7 to 10-41 M, and
compared with equal dilutions of unsuccussed 3H-thymidine
and succussed solvent. Unsuccussed 3H-thymidine solutions were prepared from an initial 3H-thymidine
solution (1 mCi/ml, specific activity 25 Ci/mmol., Amersham), by serial centesimal
dilution in pure water. Succussed 3H-thymidine
solutions and the solvent (pure water) were prepared in the same way, but
in addition, potent vertical shaking was performed between successive dilution
steps. Finally, 200 µl from each solution were added to 3 ml of scintillation
solution (Pico-Fluor 15) and counted in a ß-liquid scintillation analyzer
(Packard).
2. 7. DETERMINATION OF SPECIFIC ANTI-Tg IgM AND IgG TITRES
The titres of specific antibodies against porcine Tg
were determined in sera by indirect enzyme-linked immunosorbent assay (ELISA)
technique. Microtitre plates (Immunoplates II, NUNC, Roskilde, Denmark) were
coated with a solution of porcine Tg at 10 µg/ml in phosphate buffered saline
(PBS) at pH 7.2, and the plates were incubated overnight at 4° C. The plates
were washed three times with PBS containing 0.1% Tween 20 (V/V); then 100
µl of chicken plasma diluted by half from 1/20 were added to the plates and
incubated at 37° C for 1 h. The plates were washed three times. For the determination
of anti-Tg IgM, 100 µl of horseradish peroxidase-labelled anti-chicken IgM
conjugate (Bethyl Laboratories, Montgomery, AL) was added and the plates were
incubated at 37° C for 1 h. After the last washing, the enzyme substrate,
o-phenylenediamine (Sigma) was added and the plates were icubated for 15 min
at room temperature. The absorbance was measured at 450 nm using a Multiskan
photometer (Flow Laboratories, Marseille, France). For the determination of
anti-Tg IgG, 100 µl of alkaline phosphatase-labelled anti-chicken IgG conjugate
(Sigma) were added and the plates were incubated for 1 h at 37° C. After the
last washing, 4-nitrophenylphosphate (Sigma) was added and the plates were
incubated for 30 min at 37° C. The absorbance was measured at 405 nm. The
titres of anti-Tg IgG or IgM were defined as the reciprocal of the plasma
dilution giving a absorbance equal to 1.0 by indirect ELISA. Results were
expressed in titre log.
The same technique was used to measure anti-KLH antibodies.
Briefly, microtitre plates were coated with 100 µl/well of a KLH solution
(10 µg/ml PBS) and incubated overnight at 4°C. Then, the plates were washed
three times with PBS containing 0.1% Tween 20 (V/V). Afterwards, 100 µl of
chicken plasma dilute at 1/40 were added to each well and the mixture held
under 37° C for 1 h. The plates were rinced three times. Then 100 µl of peroxydase-conjugated
affinipure rabbit anti-chicken IgG Fc fragment specific (Jackson ImmunoResearch
Laboratories) dilute at 1/1000 in PBS-0.1% Tween 20 were added to the wells.
The plates were incubated again for 1 h at 37° C. After three washings, 100
µl of the enzyme substrate termed o-phenylenediamine (Sigma) were added to
the wells and the plates were allowed to incubate 5 min at room temperature.
The enzymatic reaction was stopped by adding 50 µl/well of H2SO4 and the absorbance
was measured at 490 nm. The titres of anti-Tg IgM or IgG antibodies were defined
as for anti-Tg antibodies and the results were expressed in the same way.
The specificity of anti-Tg antibodies was checked by
either an inhibition technique or a cross reaction test, using self-chicken
(ovalbumin: OVA, ß-actin: ACT, myosin: MYO) or foreign (BSA, porcine insulin:
INS, porcine Tg: Tg) antigenic proteins (Sigma). For the inhibition technique,
the sera collected from 38 day-old chickens were dilute according to their
titres and they were incubated with 2 µg/ml of the different proteins overnight
at 4° C. Then an ELISA test using either porcine Tg or KLH as the antigen
was performed on each treated serum in comparison with the corresponding untreated
serum. The cross reaction consisted in testing the binding capacity of the
above-listed antigens to sera collected at d20, d29, d38 and d47, by means
of ELISA test.
2. 8. DETERMINATION OF HORMONES
The plasma concentrations of CORT (ng/ml) were measured
by competitive protein-binding assay. This technique was previously made suitable
for chicken plasma samples (Buckland et al., 1974). Intra and inter-assay coefficients of variation were
3.1 and 5.6% respectively. The sensitivity of the assay was 0.05 ng/ml. ACTH
was assessed using a RIA kit (ACTH K-PR) purchased from CEA (Paris, France)
(Ramade et al., 1985). Intra- and
interassay coefficients of variation were 7.5 and 9.0 % respectively ; the
sensitivity of the assay was 10 pg/ml. Plasma MLT concentrations (pg/ml) were
determined by RIA according to the method developed by Rollag and Niswender
(1976) and adapted to chicken by Cogburn et
al. (1987). Intra and inter coefficients of variation were 14 and 12%
respectively. The sensitivity of the assay was 3 pg/ml.
2. 9. ENZYMATIC ACTIVITIES
NAT and HIOMT activities were measured according to the
techniques of Voisin and Colin (1986) and Voisin et al. (1988), respectively. Individual pineal glands were homogenized
by sonication in 60 µl sodium phosphate buffer (0.05 M, pH 7.9). The enzyme
substrates [20 µl tryptamine (20 mM), 20 µl of 3H-acetylcoenzyme
A and H-acetylcoenzyme A mixture (specific activity: 4 Ci/mole)], 20 µl of
sodium phosphate buffer (0.05 M, pH 7.9) and 40 µl of pineal homogenate, for
a total volume of 100 µl were introduced in Eppendorf tubes. The blank Eppendorf
were filled with 20 µl of tryptamine (20 mM), 20 µl of a mixture of 3H-acetylcoenzyme
A and H-acetylcoenzyme A (specific activity: 4 Ci/mole) and 60 µl of sodium
phosphate buffer (0.05 M, pH 7.9), total volume 100 µl. The Eppendorf contents
were mixed and incubated for 30 min at 37° C. Thereafter, 1 ml chloroform
was added into the tubes at 4° C to stop the reaction. Then the tubes were
shaken, centrifuged (1000 g, 1 min) and the upper phase discarded. The chloroform
phase containing the reaction product(s) was washed with 200 µl sodium phosphate
buffer , centrifuged (10,000 g, 1 min) and the upper phase discarded. The
chloroform phase (500 µl) was evaporated (2 h, 50° C), 7 ml of scintillant
added to the residual powder and the radioactivity measured in a ß scintillation
counter.
For HIOMT activity, 100 µl containing the substrates
[25 µl N-acetylserotonine (25 mM), 25 µl of a mixture of 3H-S-adenosyl-methionine
and H-S-adenosyl-methionine (specific activity: 25 Ci/mole)], 40 µl borate
buffer (0.3 M, pH 10) and 10 µl of pineal homogenate. In blank tubes, 25 µl
of N-acetylserotonin (25 mM), 25 µl of a mixture of 3H-S-adenosyl-methionine
and H-S-adenosyl-methionine (specific activity: 25 Ci/mole) and 50 µl borate
buffer (0.3 M, pH 10) were mixed. The tubes were treated similarly to those
used to determine NAT activity, except that the reaction was stopped using
1 ml of chloroform and 20 µl of borate buffer.
2. 10. STATISTICAL ANALYSIS
The data represent mean ± S.E.M and were processed by
two-way ANOVA, followed by one-way ANOVA and Mann-Whitney tests.
2. 11. HISTOLOGICAL CONTROLS
The birds were sacrificed at the end of the experiments.
After autopsy, the absence of bursal remnants was ascertained by thorough
ocular inspection and Cleveland-Wolff stained serial sections of the whole
cloacal region were examined to verify completeness of bursectomy. Only the
animals which met this creteria were used.
3. 1. PITUITARY-ADRENAL RESPONSES TO ETHER STRESS
In the first protocol (Figure 1), ACTH and CORT levels
were at resting values prior to ether stress application, irrespective of
experimental groups. Bursa-intact chickens (N) exhibited strong hormonal responses
after ether vapour exposure. No ACTH response was noticed in bursectomized
birds (Bx) who rather raised a significant CORT response. The effectiveness
of bursin treatment in reversing the effects of bursectomy appeared inversely
proportional to the amount of the tripeptide administered: 100 µg induced
a moderate increase in CORT but not ACTH levels and only after stress application,
while either 5 CH or 7 CH restored quite normal pituitary-adrenal responses.
Figure 1. Plasma ACTH
(A) and Corticosterone (B) levels before (white columns) and after (dark columns)
ether stress application to sham-operated (N), bursectomized (Bx) and bursectomized
chickens supplemented with decreasing amounts of bursin: 100 µg (Bx+Bµ) or
100 pg (Bx+Bp) or 100 fg (Bx+Bf) . +P<0.01 vs Rest (white columns);
*P<0.01 vs Bx
3. 2. HORMONAL AND SPECIFIC HUMORAL IMMUNE RESPONSES
TO IMMUNIZATION
In the second protocol, 20 to 47 day-old chickens underwent
an immunization program to check the hormonal (ACTH, CORT, MLT) and specific
antibody (IgM, IgG) responses. The results are outlined in Figures 2, 3 4.
Regardless of experimental groups, hormonal levels (Figures 2A, B; 3A; 4A,
B, C) were at resting values prior to immunization (d20) and hardly shifted
9 days after the first antigen challenge (d29). However, in sham-operated
birds (N or N+S), hormonal responses reached a zenith at d38 and finally dropped
to basal values after at d47. Assessed in parallel to endocrine
Figure 2. Hormonal (A,
B) and specific antibody responses (C, D) after immunization with porcine
Tg. Sham-operated birds (N) or bursectomized chickens (Bx) treated in ovo
with different amounts of bursin (Bx+Bµ; Bx+Bp; Bx+Bf) were sequentially immunized
at 21, 30 and 39 days of age. Then plasma levels of ACTH (A) and corticosterone
(B), as well as the serum titers of anti-Tg IgM (C) and anti-Tg IgG (D) were
measured the day before (d20: white columns) and at the age of 29 (d29: dotted
columns), 38 (d38: hatched columns) and 47 (d47: dark columns) days. +P<0.01
vs d20; *P<0.01 vs Bx.
parameters, the specific humoral immune response (Figures 2C, D; 3B, C; 4 D) presented a different feature: especially in sham-operated samples, not only antibody production arose earlier, but it varied increasingly from the first to the third immunization.
Figure 3. Corticosterone
(A) and specific anti-Tg IgM (B) and IgG (C) responses to immunization against
porcine Tg as measured in sham-operated (N) and bursectomized chickens supplemented
with either the saline (Bx+S) or 100 fg (Bx+Bf) or a high dilution (5 x 10-27
g) of bursin. The birds were sequentially immunized against porcine Tg at
the age of 21, 30 and 39 days and Corticosterone and antibody levels were
evaluated the day before the first immunization (d20: white colums) and at
the age of 29 (d29: dotted columns), 38 (d38: hatched columns) and 47 (d47:
dark columns). +p<0.01 vs d20; *p<0.01 vs Bx. ND: Non-determined antibody
titers (d20 for IgM, d20 and d29 for IgG).
On the other hand, hormonal levels remained steadily
low in bursectomized chickens (Figures 2A, B; 3A; 4A, B, C) who also failed
to mount specific antibody production in spite of repeated immunization (Fig.
2C, D; Figures 3B, C; 4D) and whether they had received the saline or the
control tripeptide (Figure 4D).
Figure 4 a:.
ACTH (A), corticosterone (B), melatonin (C) and anti-Tg IgG (D) responses
to immunization against porcine Tg. Seven experimental groups were used (N,
N+S, Bx, Bx+S, Bx+Pf, Bx+Bf, Bx+B-27. The animals were immunized at the age of 21, 30 and 38
days. Blood samples were collected the day before the first immunization (d20:
white columns) and at the age of 29 (dotted
columns), 38 (hatched columns) and 47 (dark columns) to check the plasma levels
of hormonal (ACTH,corticosterone, melatonin) and specific antibody (IgG) responses.
+P<0.01
vs Bx; *P<0.01 vs Bx+S.
The
administration of 100 µg of bursin could no longer reverse of the alterations
caused by bursectomy. Conversely, either discrete amounts (5 CH, 7CH) or a
high dilution (15-20 CH pool) of bursin induced the recovery of normal endocrine
and specific humoral immune performances in bursectomized recipients.
The specificity of anti-Tg antibodies was ascertained
by an inhibition technique (Figure 4E) or a cross reaction test (Figure 4F)
using either chicken self-proteins (OVA, ACT, MYO) or xeno-antigens (BSA,
INS, Tg). Clearly, at the exclusion of the other proteins used, porcine Tg
specifically reacted with the tested sera.
Figure 4 b. The specificity
of anti-Tg IgG was assessed either by an inhibition technique (E) or a cross
reaction test (F) using self-chicken (ovalbumin: OVA, myosin; MYO, ß-actin:
ACT ) or foreign (BSA, porcine insulin: INS, porcine Tg: Tg) proteins. In
the inhibition technique, the sera collected from 38 day-old chikens were
tested. The cross reaction test included sera harvested at the age of 20,
29, 38 and 47 days. .P<0.01 vs other proteins.
In the study designed to elucidate the nature of endocrine
responses triggered by porcine Tg (experiment 5), bursa-intact chickens exhibited
the same profile of CORT response (Figure 5A), irrespective of the sensitizing
agent (porcine Tg or KLH): CORT levels increased significantly at d35 and
crested at d38. Even though antibody responses (IgG) started earlier (d29)
than endocrine responses (d35), KLH- and porcine Tg-challenged chickens displayed
the same feature of humoral immunity: IgG levels rose from prime to third
immunization (Figure 5B). It is worth noting that in each case (KLH or porcine
Tg), the humoral immune response (IgG) was contemporary of the endocrine response
(CORT), both cresting simultaneously.
Figure 5. CORT (A) and
IgG (B) responses of bursa-intact chickens sensitized to either keyhole limpet
hemocyanin (KLH) or porcine Tg. Both parameters were measured the day before
immunization (d20: white columns) and at the age of 29 (dotted columns), 36
(hatched columns) and 38 (dark columns) days.*P<0.01 vs d20. The samples
comprised 18 and 17 chickens for KLH and porcine Tg respectively.
3. 3. CIRCADIAN RHYTHMS OF THE PITUITARY-ADRENAL AND
PINEAL ACTIVITIES
In the third protocol (Table 1; Figures 6; 7), birds
experienced a 12L-12D light-dark regime.Sham-operated birds (N) exhibited
diurnal rhythms of plasma ACTH (Figure 6A), CORT (Figure 6B) and MLT (Figures
6C; 6D), with low light-time levels and significantly higher night-time values,
in phase with light-dark cycle. Hence, broadpeaks were recorded during the
dark phase (ACTH: 75.5 ± 3.42 pg/ml and CORT: 8.9 ± 0.25 ng/ml at 2100; MLT:
154.84 ± 8.21 pg/ml at 0000), whereas trough levels occurred during photophase
(ACTH: 46 ± 3.49 pg/ml; CORT: 3.46 ± 0.28 ng/ml;
MLT: 14.5 ± 3.06 pg/ml at 1200). Pineal and ocular MLT
contents (Table 1) were also higher at night (13960 ± 2514 pg/pineal and 612
± 102 pg/eye at 0000) than during daytime (1662 ± 349 pg/pineal and 292.5
± 74.8 pg/eye at 1200).
TABLE 1. Day/night differences in melatonin levels
________________________________________________
Organ
Time
________________________________________________
1200 0000
_______________________________
Pineal gland
1,662 ± 349 13,960±
2514*
Retina 292 ± 75
612 ± 10*
Plasma 14.54 ± 3.06
154.84 ± 8.21*
________________________________________________
Melatonin concentration measured at 1200 and 0000 in the
pineal
gland (pg/pineal), retina (pg/retina) and plasma (pg/ml)
of 13 intact chickens P < 0.01
vs 1200.
This
pattern of variation was in keeping with the rhythm of pineal NAT (Figure
6E) activity (1.3 ± 0.14 nmol/pineal/h at 1200 versus 24 ± 2.2 nmol/pineal/h
at 0000). On the other hand, HIOMT (Figure 6F) did not vary significantly
between the photo- and scotophase (13.62 ± 1.43 nmol/pineal/h at 1200; 18.05
± 1.64 nmol/pineal/h) and irrespective of experimental groups. After bursectomy
(Bx), the daytime levels of plasma ACTH and CORT. (Figure 6A, B) were no longer
significantly different from nighttime ones (ACTH: 38 ± 0.46 to 47 ± 2.82
pg/ml; CORT: 4.24 ± 0.32 to 4.44 ± 0.29 ng/ml). Persistent diurnal rhythms
were noticed in plasma MLT (5.7 ± 0.38 pg/ml at 1200 versus 65.77 ± 2.78 pg/ml
at 0000) as well as NAT activity (0.73 ± 0.07 nmol./pineal/h at 1200 versus
5.13 ± 0.28 nmol./pineal/h at 0000), even though reduced by 50% in magnitude.
In our attempt to reverse the effects of bursectomy, different amounts of
bursin were administered in the yolk-sack of 6 and 9 days old bursectomized
embryos.
Figure 6. Pituitary (A), adrenal (B) and pineal (C, D, E, F) daily
activities measured at daytime (white columns) and at night (dark colmuns).
Six groups of chickens (N, Bx, Bx+Bµ, Bx+BP, Bx+Bf, Bx+B-27) were submitted
to a 12L-12D light-dark cycle. Blood samples were collected during daytime
(1200-1300) and at night (0000-0100) to measure plasma ACTH (A), corticosterone
(B) and melatonin (C, D).The pineal glands were assayed for enzymatic activities
of NAT (E) and HIOMT (F). + P<0.01
vs 12.00; * P<0.01 vs Bx.
Figure 7. Circadian rhythms of the pituitary (A, B), adrenal (C,
D) and pineal (E, F) hormones. The 7 groups of animals listed above were submitted
to a 12L-12D alternating light-dark cycle, with lights off from 0700 to 1900
(black bar below the figures) .The plasma samples were assayed for ACTH (A,
B), corticosterone (C, D) and melatonin (E, F). +P<0.01vs Bx; *P<0.01
vs Bx+S.
As results, the
highest dose of bursin (100 µg) could not induce the recovery of the daily
rhythms of plasma ACTH and CORT, whose levels remained steadily low and close
to values observed in Bx animals (Fig. 6A, B). Likewise, 100 µg of bursin
could no longer restore the normal amplitude of plasma MLT (Figure 6C). Conversely,
lower amounts of bursin (5 CH, 7 CH, 15-20 CH pool) elicited significant daily
hormonal and enzymatic rhythms, in an inverse dose-dependent manner (Figure
6A, B, C, D).
The hormonal parameters were also assessed every 4 h
during a single light-dark cycle (Figure 7). Bursa-intact birds displayed
pronounced circadian rhythms of plasma ACTH (Fig. 7A, B), CORT (Figure 7C,
D) and MLT (Figure 7E, F), phase-locked with photoperiod and reaching a sharp
peak at midscotophase. Bursectomy completely abolished circadian rhythms of
the pituitary-adrenal hormones (Figure 7A, C), whereas MLT rhythm persisted,
though markedly reduced in height (Figure 7E). Once more, neither the control
tripeptide (Figure 7A, C, E) nor the saline (Figure 7B, D, F) could correct
the effects of bursectomy. Administration of 100 µg of bursin has been reported
also harmless in doing so (Youbicier-Simo, 1990). On the other hand, lower
amounts of bursin (5 CH, 7 CH, 15-20 CH pool) allowed restoration of quite
normal hormonal rhythms, in an inverse dose-dependent manner (Figure 7B, D,
F).
3. 4. SERIAL DILUTIONS OF 3H-THYMIDINE
In the fourth protocol, we demonstrated that in sequentially
dilute 3H-Thymidine solutions, the radioactivity decayed linearly,
without showing any difference between succussed and unsuccussed solutions
(table 2).
__________________________________________________________
3H-Thymidine
(cpm) was quantified in different concentrations of succussed thymidine solutions
ranging from 10-7 to 10-41 M and compared to unsuccussed thymidine and solvent.
The data represent means ± SEM of three independent experiments. As result,
a plummet in 3H-Thymidine concentration was recorded and no residual
tritiated compound could be detected above 10-15 M.
4.1. BURSECTOMY AND EMBRYONIC MORTALITY
Our experimentation lasted 6 years during which more
than 10.000 chicken embryos have been studied. In the sham-bursectomized groups,
fetal loss (5-10%) was essentially restricted to the end of the incubation
period. A possible explanation to this time-limited mortality is that the
end of incubation corresponds to the preparation of hatching and represents
a critical period during which the conditions of an extremely severe stress
are gathered, weakening the fetus (Bauman and Bauman, 1977). Besides, two
main critical periods characterized by a high death rate were identified during
the development of the bursectomized chicken embryo: 20 to 30% of the operated
embryos died between the day of bursectomy (4 th day of incubation) and the
first day of in ovo treatment (6 th day of incubation), whereas
40 to 65% mortality occurred around hatching. A third critical phase arised
during the couple of weeks following hatching, due to either cloacal malformations
or immunodepression (Belo et al.,
1985). Finally, we recorded 8-10% survival two weeks after hatching. Performing
surgical bursectomy at 60 h of embryonic life, Fitzsimmons et al. (1973) reported 6% survival after
hatching; Belo et al. (1985) and
Corbel et al. (1987) reported 5
and 7 % survival respectively, operating on 5 day-old chicken embryos. Grafting
of 9.5 day-old chicken bursae (period of colonization of the bursa by B stem
cells) does not improve the survival of bursectomized recipients (Ramade et al., 1985; Abdul-Karim et al., 1987), whose mortality rather got
worse after the twofold administration (6 th and 9 th days of incubation)
of bursin in the yolk sack. Finally, embryo handling appears as the prominent
factor of mortality.
4.2. BURSECTOMY AND HUMORAL IMMUNITY
In order to evaluate the physiological consequences of
both embryonic bursectomy and in ovo
treatment with bursin, we tested the ability of bursectomized and bursin-treated
bursectomized chickens to respond immunologically and hormonally to some environmental
stimuli such as ether vapour, antigen challenge and photoperiod.
Control birds exhibited strong and increasing immunoglobulin
production (IgG) during the course of immune response. These antibodies were
specific to porcine Tg, since they reacted with neither self-chicken proteins
(OVA, ACT, MYO) nor foreign antigens (INS, BSA). Unlike their bursa-intact
counterparts, bursa-lacking chickens failed to raise specific anti-Tg antibodies,
in spite of repeated immunization. These data are consistent with earlier
reports indicating that bursa-lacking animals are able to produce immunoglobulins
of the IgM, IgG and IgA classes, but fail to mount specific antibody responses
against various antigens, despite iterative immunization (Jankovic et
al., 1977; Granfors et al.,
1982; Jalkanen et al., 1983). This lack of specificity
is correlated with decreased number of Ig bearing cells: IgG positive cells
in the spleen, thymus and blood (Jalkanen et
al., 1984). The finland team of Toivanen also demonstrated that the number
of B-cell clones is strikingly reduced in bursectomized chickens (Mansikka
et al., 1990). This oligoclonality of the
B-cell compartment is paralleled by a 10 fold decrease in serum IgG titres,
IgM and IgA levels remaining unchanged (Jalkanen et al., 1983). It is worth noting that our results match these data,
at least as far as the serum titres of IgG are concerned. By contrast, in
bursectomized chickens, the IgM titres assessed by us appeared rather lessened.
Nevertheless, our analysis must be shaded, because the level of Ig depends
on age: in fact, if the levels of IgM, IgG and IgA are markedly low in the
10 day-old bursectomized chickens, the latter recover normal Ig titres by
the age of 10 weeks (Eerola et al.,
1983). Now, our measurements were performed half-way (3 to 7 weeks), between
10 days and 10 weeks. Evidence has been presented that at protein level, the
isoelectric spectrum of immunoglobulins derived from bursectomized chickens
displays normal gamma chains, but altered light chains, due to predominance
of basic versus deficit in acid amino acids, which results in reduced antigen-antibody
binding affinity (Granfors et al., 1982,
Jalkanen et al., 1984). In addition,
a low Ig gene conversion rate (V-J and V-D-J gene rearrangements) leading
to a poorly diversified immunoglobulin repertoire has been reported in bursectomized
chickens (Mansikka et al., 1990). Collectively, these data suggest that the bursal microenvironment
plays a crucial role in the elaboration and diversification of the specific
antibody repertoire. These bursa-dependent events might occur very early during
embryonic life, probably at the beginning of the colonization of bursa follicles
by B precursors cells (Weill and Reynaud; 1986, Reynaud et al., 1992). The bursa anlage develops
on the 5 th day of embryonic life and is invaded by a single wave of B stem
cells between the 8 th and the 14 th day of incubation (Houssaint et al., 1976; Lassila et al., 1978; Le Douarin et al., 1985). We performed surgical bursectomy
at 80 h of embryonic development, so as to obtain complete and permanent B-deficient
animals.
4.3. BURSECTOMY AND IMMUNO-NEUROENDOCRINE RESPONSIVENESS
If the bursa of Fabricius is undoubtlessly a key organ
of the B immune component in Birds, it has been for a long time suspected
to also serve various neuroendocrine functions: reduced CORT levels and enlarged
adrenals, have been observed in newly-hatched chicks bursectomized at 68 h
of embryonic life (Pedernera et al.,
1980); Bursectomy performed in 2 week-old chicks increases the adrenal ascorbic
acid response to ACTH (Perek and Eckstein, 1959, Perek and Eilat, 1966), whereas
the hyperglycemic response following intramuscular injection of ACTH is lessened
(Freeman, 1971); CORT levels increase after bursectomy (Mashaly, 1984). Analogous
results have been previously obtained in our Laboratory. We reported that
early surgical bursectomy (4 th day of embryonic life) results in various
alterations in pituitary and adrenocortical functioning: ether stress-induced
ACTH and CORT stimulations can be detected more precociously in bursectomized
than in bursa-intact embryos; the non-stress responsive period of newly-hatched
bursa-intact birds does not arise in bursa-lacking chicks (Guelatti, 1990;
Guelatti et al., 1991); young bursa-lacking
chickens exhibit a smaller CORT response to stress than controls (AbdulKarim
et al., 1987); the delayed pituitary-adrenal
responses of adenohypophysectomized chickens to Brucella abortus does not
occur when embryonic bursectomy preceedes hypophysectomy (Baylé et
al., 1991). In line with our previous results, we now present evidence
of inability for bursa-deprived young chickens to cope with ether stress.
Thyroglobulin
(Tg) which was used by us to sensitize the chickens is also the endogenous
precursor of thyroid hormones (Teppermann and Teppermann, 1987), and the latter
are correlated to CORT during the course of immune response (Besedovsky et al., 1975; Trout et al., 1988). Unlike Tg which is a bioactive
compound, KLH is a T-dependent antigen devoid of any pharmacological activity.
We found that bursa-intact chickens sensitized to porcine Tg displayed the
same profiles of pituitary-adrenal and humoral immune responses as their KLH-treated
counterparts. The same feature of MLT response was recorded when immunizing
bursa-intact chickens against porcine Tg or KLH (data not shown). Accordingly,
it can be reasonably inferred that the changes of ACTH, MLT and CORT levels
subsequent to porcine Tg treatment were not modulated by thyroid hormones
derived from the sensitizing agent (porcine Tg), but were strictly linked
to the immunization phenomenon. The fact that porcine Tg failed to induce
noticeable endocrine answers in bursa-lacking chickens supports this point
of view.
Therefore,
the physiological meaning of the concomitance of hormonal and antibody responses
to porcine Tg should be discussed in the context of two-way communication
between the immune and neuroendocrine systems. The hormonal response to antigen
challenge is always contemporaneous with humoral immunity: in rats or mice
primed intraperitoneally with three antigens, concomitant peaks of CORT and
antibody responses occurred 5 to 6 days after immunization (Besedovsky et al., 1975); in the same way, both responses
crested simultaneously 3 h after intravenous administration of Brucella abortus to immature chickens (Trout
et al., 1988). We recorded analogous
pituitary-adrenal and IgG responses when immunizing chickens against porcine
Tg: ACTH and CORT levels, as well as IgG titers crested 18 days after prime
immunization (d38). It is worth noting that in the aforementioned studies
(Besedovsky et al., 1975; Trout
et al., 1988), the delay of onset between
hormonal and antibody responses was short (several minutes to three days).
This was not the case in our experiments: the antibody response arose earlier
(d29) than the hormonal response which occurred only 9 days later (d38). This
discrepancy probably comes from methodological differences, leading to specific
response kinetics. In the experiments of Besedovsky et al. (1975) or Trout et al. (1988), the antigens were injected
free of adjuvant and directly into the general circulation (intraperitoneally
or intravenously); hence they were rapidly conveyed into the secondary lymphoid
organs to induce antibody production and cytokine release. In our study, not
only porcine Tg was mixed with either complete (prime immunization) or incomplete
(second and third immunizations) Freund adjuvant, but it was applied subcutaneously.
As a result, the antigen molecules diffused slowly and had to pass through
the lymphatic circulation before reaching the site of immune response. Some
cytokines such as IL-1 or IL-2 have potential to increase blood glucocorticoid
level via stimulation of the HPA axis (Glick, 1984b; Besedovsky et
al., 1981; Lilly and Gann, 1992; Hu et
al., 1993). Considering above arguments and despite induction of humoral
immunity at d29, it is likely that the level of cytokines reached at d29 was
not high enough to feedback on the HPA axis and elicit noticeable ACTH and
CORT responses. Accordingly, we assume that after prime immunization, these
responses had been initiated later than d29, at a moment when the effective
concentration of cytokines was attained. A few days after subcutaneous administration
of porcine Tg, we observed inflammatory nodules at the site of immunization.
Evidence has been presented suggesting that cytokines released by inflammatory
cells play a major role in HPA axis immunoregulation (Lilly and Gann, 1992;
Besedovsky and Del Rey, 1987). Therefore, an alternative explanation to the
lack of endocrine responses at d29 is that these responses were missed, because
they had been induced earlier than d29 by inflammatory cytokines.
Another
distinctive feature of our results comes from the fact that endocrine and
antibody responses were associated to repeated rather than unique immunization
as reported by other authors (Besedovsky et
al., 1975; Trout et al., 1988).
Especially, CORT crested at d38, whether this sampling point was assessed
after the second (experiments 2, 3, 4, 5) or the third (experiment 6) antigen
challenge. Moreover, we noticed either a decline (experiment 2, 3, 4, 5) or
a peak (experiment 6) of CORT following the third immunization. Also, the
CORT level measured at d36 was half-way between the values at d29 and d38.
For these reasons, the hormonal profiles might depend, not on iterative immunization,
but on the time elapsed after prime immunization. This explanation seems more
in agreement with the assumption of retarded arousal of ACTH and CORT responses
(after d29). The concomitance of the peaks of CORT and IgG (d38) can be intrepreted
as part of an immuno-neuroendocrine regulatory loop: the activation of B-cells,
in conjunction with T-cell activation, induces the release of cytokines which
increase glucocorticoid level via the HPA axis (Besedovsky et al., 1981; Lilly and Gann, 1992; Hu
et al., 1993); this is a possible explanation
to the peaks of ACTH and CORT observed at d38. This circuit is enhanced by
MLT (Maestroni, 1993) which have been demonstrated by us to crest contemporaneously
with pituitary-adrenal hormones. In turn, increased glucocorticoid levels
inhibit MLT rise (Besedovsky et al., 1975; Poon et al.,
1994), and also impede cell-mediated immunity, leading to both reduction of
cytokine levels and decline of CORT level (Lilly and Gann, 1992; Hu et al., 1993; Besedovsky et al., 1985) as observed by us at d47.
Finally, iterative immunization seemingly played the role of amplifying endocrine
and immune responses.
However,
the HPA axis and the pineal gland not only mediate adaptation to nociceptive
situations, but they are also sensitive and responsive to light stimuli which
acts as zeigteber on biological rhythms in most Vertebrates (Binkley, 1993).
Therefore, we wondered if the bursa of Fabricius possibly influences the circadian
rhythms of both HPA and pineal gland in the chicken.
4.4. BURSECTOMY AND CIRCADIAN RHYTHMS OF HPA AXIS AND
PINEAL GLAND
The circadian activity of the pituitary-adrenal axis
is governed by the rhythmic activity of CRF-containing neurons of the hypothalamus
(Peczely and Antoni, 1984; Jozsa et al., 1984). These CRF-neurons project in the median eminence, in
the vicinity of pituitary portal capillaries where CRF is rhythmically released
(Peczely and Antoni, 1984; Jozsa et
al., 1984) and triggers the circadian secretion of ACTH and downstream
CORT. In the present study, bursa-intact chickens exhibited broad circadian
rhythms of ACTH and CORT under a 12L-12D light-dark cycle. Some reports indicate
that lesioning the hypothalamic paraventricular nucleus in the rat (Makara
et al., 1981) or the suprachiasmatic nucleus
in the pigeon (Bouillé and Baylé, 1973) abolishes the circadian variations
of plasma ACTH and CORT. Now the withdrawal of the bursa anlage from 4 day-old
chicken embryos was also accompanied by the suppression of the daily rhythms
of plasma ACTH and CORT in young chickens, despite exposure to a 12L-12D light-dark
regime.
The
daily synthesis and release of MLT is catalyzed in vivo by two key enzymes,
NAT and HIOMT (Binkley et al., 1973).
In 8 week-old chickens raised under 12L-12D light-dark cycle, pineal NAT and
MLT night-time levels are respectively 27 and 10 fold higher than light-time
values, whereas HIOMT activity varies by 20 % only (Binkley et al., 1973). Likewise, ocular and blood
MLT levels display prominent daily rhythms with a midscotophase crest (Cogburn
et al., 1987). Our control chickens
exhibited similar patterns of enzymatic and hormonal rhythms: night/daytime
ratios were 20, 8, 2 and 10 for pineal NAT activity, pineal MLT content, and
ocular and circulating MLT, respectively. Little change occurred in HIOMT
activity, probably due to a slow turnover of this enzyme (Voisin et al., 1988). Very striking is the observation
that in bursectomized chickens, the magnitude of NAT and MLT rhythms was markedly
reduced, in spite of persistent cyclicity. Phototransduction is anatomically
supported by a complex network comprising several elements: photoreceptors
(retinal, hypothalamic, pineal) perceive light information and convey it either
directly or via the suprachiasmatic nucleus (SCN) to the pineal gland where
the message is converted into MLT (Binkley, 1993). The visual suprachiasmatic
nucleus (equivalent of mammalian SCN) is connected to the pineal gland through
sympathetic catecholaminergic fibers and governs the circadian release of
noradrenaline in the vicinity of pinealocytes (Cassone et
al., 1990). Noradrenaline turn-over is higher during the photo- compared
to scotophase (Cassone et al., 1990). The activation of a-2 adrenergic receptors on pinealocytes upon daytime increase in noradrenaline
level inhibits the synthesis of NAT molecules and, therefore, MLT production,
via an intracellular increase of cAMP (Voisin and Colin, 1986; Bylund et
al., 1988). Since the amplitude of pineal NAT activity and MLT production
is controlled by the rhythmic delivery of noradrenaline, itself driven by
the circadian function of the vSCN (Cassone et
al., 1990), the vSCN-SCG-pineal complex appears as the most probable locus
of interferences between bursal signals (or the absence of bursal signals)
and pineal rhythms. This hypothesis is strengthened by the fact that the excision
of the bursa anlage (4 th day of embryonic life) preceeded the beginning of
pineal sympathetic innervation which occurs by day 20 of embryonic life (Wight,
1971), as well as the onset of pineal NAT and MLT rhythms which are observed
in 18 day-old embryos (Binkley and Geller, 1975). Similarly, the chronology
of the onset of bursal and pituitary-adrenal functions might help understanding
how the precocious influence of the bursa of Fabricius on pituitary-adrenal
functioning occurs: the bursa anlage arises by the third day in the embryo
(Toivanen et al., 1981); it was
excised (4 th day of embryonic life) prior to the onset of the HPA axis functioning
which in the developing chicken embryo occurs during the second half of embryonic
phase (Scanes et al., 1987). Therefore,
it is likely that as a result of precocious bursectomy, the normal development
of pituitary-adrenal activities was hindered, due to the lack of adequate
inductive bursa cue (s).
However,
the exact locus of the interferences between bursa signals and both the HPA
and the pineal gland have yet to be identified. The studied systems (bursa
of Fabricius, HPA and pineal gland) arise during the embryonic phase which
in chickens is also the critical period of sexual differentiation of the brain
(Wilson and Glick, 1970). Accordingly, the mechanisms of brain development
are likely to be involved in the functional maturation of bursa-pituitary-adrenal-pineal
interrelationships. In fact, during the critical period, sex steroids can
imprint parts of the brain that are associated with the cyclic control of
hormonal release in such a way as to prevent their rhythmic function (Pilgrim
et al., 1994). Since embryonic bursectomy
leads to significantly increased plasma testosterone levels (Pedernera et
al., 1980; Ramade et al., 1986),
such a rise might affect the cyclic activity of hypothalamic pacemakers. Among
the latter is the SCN neurally coupled to CRF-containing nuclei which govern
the circadian release of ACTH and CORT (Peczely and Antoni, 1984; Jozsa et al., 1984) and to the pineal gland which
secretes MLT in a cyclic manner (Binkley, 1993). As working hypothesis, it
can be assumed that similar mechanisms occur in bursectomized embryos in the
absence of specific bursal cue (s); in intact embryos, such signal (s) must
normally prevent the unsettling of the hypothalamic and pineal pacemakers.
These
dyschrogenic effects emphasize the crucial role held by signals originating
in the bursa microenvironment in the ontogeny and functioning of immune, HPA
and pineal activities. Further support to this assertion comes from the fact
that bursectomized chickens embryonically grafted with 9 day-old embryonic
bursae recover normal immune responsiveness
and normal levels of plasma CORT (Abdul-Karim et al., 1987) and testosterone (Pedernera et al., 1980). In this regards, we demonsrated that the bursa-derived
signal termed bursin is an important mediator of bursa-dependent functions.
4.4. BURSIN AS MEDIATOR OF BURSA-DEPENDENT FUNCTIONS:
EFFECTIVENESS OF HIGHLY DILUTE BURSIN
Differents concentrations of bursin were tested, aimed
at reversing the effects of bursectomy. In
ovo administration of very low
doses (5 CH, 7 CH) of bursin to bursectomized chickens allowed recovery of
the ability to cope with ether stress, antigen challenge and restored normal
pituitary-adrenal and pineal rhythmicity. Chorio-allantoic grafting of bursal
rudiment from 9.5-day-old donor embryos has been reported to alleviate gonadal
(Pedernera et al., 1980) and adrenal
(Abdulkarim et al., 1987) changes
caused by bursectomy. Also bursa extracts have ben reported to restore specific
humoral immunity in bursectomized chickens (Baba and Okuno, 1976). Kuznik
et al. (1988) demonstrated that peptides
from bursal origin correct both immunity and homeostasis in bursectomized
chickens. Increasingly, the data strengthen the assumption of specific inductive
properties for minute doses of bursin on immune and neuroendocrine functions
during embryonic life: native as well as synthetic bursin (Lys-His-Gly-NH2)
stimulates an intracellular increase of cAMP and cGMP in the human Daudi B
cell line, at threshold concentrations of 0.1 to 1 µg/ml (Audhya et
al., 1986). On the other hand, either the inverse sequence of bursin (Gly-His-Lys-NH2)
or other variants of this tripeptide (Gly-His-Lys; Lys-His-Gly) appear poorly
inductive, and only when administered in massive amounts (Audhya et al., 1986; Lassila et al., 1989), which makes this action
physiologically irrelevant. Using either the saline or a control tripeptide
with unknown biological activity (Trp-Leu-Leu-NH2), we could not
overcome the effects of bursectomy; in
ovo administration of 100 µg of bursin was no longer effective. Hence,
bursin worked in an inverse dose-dependent manner, the lower doses being the
most effective. Underlying mechanisms remain unraveled. Bursin triggers intracellular
increase of cAMP and cGMP (Goldstein et al., 1977; Audhya et al.,
1986). Like homologous tripeptides (Gly-His-Lys, His-Gly-Lys) known to enhance
cell growth, bursin contains histidine which binds to and promote copper uptake
in a variety of cells (Pickart and Thaler, 1973; Pickart, 1981). Bursin is
likely a growth factor (Lassila et al.,
1989).
Much
more striking is that highly dilute bursin (15-20 CH pool) improved the performances
of bursectomized chickens, to the same extent as did 7 CH of bursin. Highly
dilute bursin seemed to transmit specific "information" to bursectomized
recipients. Bursin's specific inductive properties were ascertained by replicating
the data pertaining to the immunization protocol: the previous results (Youbicier-Simo
et al., 1993) were exactly reproduced (Youbicier-Simo
et al., 1996b). Furthermore, highly
dilute bursin wholly restored normal circadian rhythms of the pituitary-adrenal
axis (Youbicier-Simo, 1994; Youbicier-Simo et al., 1996b) and pineal gland (Youbicier-Simo,
1994; Youbicier-Simo et al., 1996a).
Another striking observation is that the pharmacological effect induced by
the saline in saline-supplied chickens (N+S) was suppressed after embryonic
bursectomy: in figure 4 B, the bursa-intact chickens supplimented with the
saline (N+S) exhibited a slightly higher CORT response than their untreated
counterparts; on the other hand, this effect did not occur when bursa-lacking
chickens (Bx) received the saline (Bx+S). How do highly dilute solutions work
remains enigmatic, since they are theoretically devoid of active material
compounds. It has been shown by nuclear magnetic resonance that the structure
of high dilutions is different from that of solvents (Demangeat et al., 1992). Several theories have been
put forward, but a deciding factor of the efficiency of high dilutions
seems to lie in the way such media are prepared, using sequential centesimal
dilution steps with potent vertical stirring between successive steps. We
demonstrated that in sequentially diluted 3H-thymidine solutions,
radioactivity decayed linearly, without showing any difference between succussed
and unsuccussed solutions (table 2). This testifies to a homogeneous molecular
dispersion as result succussion, therefore precluding the assumption of heterogeneous
molecular distribution sustained by the theory of clusters. We suggest that
a non-molecular specific information signal corresponding to the original
molecule (bursin) is conveyed to the recipient organism (Bastide and Lagache,
1992). Indeed, the activity of high dilutions is sensitive to electromagnetic
fields (Hadji et al., 1992) and had been transferred to unshaken water through
a coil (Endler et al., 1995) and
may be probably electromagnetically transmitted. Currently, an increasing
number of experiments aimed at substantiating the biological activities of
high dilutions are under way, and some reports are compelling (Bastide et
al., 1985; Bastide et al., 1987; Daurat et al., 1988; Jacobs et al., 1994; Reilly et al., 1994; Bastide and Boudard, 1995).
Finally,
using a relevant experimental model, we have provided evidence that a compound
found in the bursal microenvironment can functionally mimic in vivo
some biological functions of the bursa Fabricii. We assert that in
chickens, the bursa-derived signal (bursin) which is probably an ontogenic
organizer, mediates early bursa-dependent functions. The originality and novelty
of the present work lie in the underscoring of the inverse dose-dependent
effectiveness of high dilutions, in contrast with the classical dose-dependent
effect which underlies the molecularist theory. We introduce a new conceptual
trend of the information processing termed the "paradigm of signifiers";
the latter is rather based on the encoding of the "specific information"
contained in bioactive compounds by highly dilute media.
Aknowledgement.
The present work was supported
by grants from Dolisos Laboratories (Paris).
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F., and Baylé, J.D. (1987) Development of basal and stress-induced adrenocortical
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