The role of neuroendocrine immune interactions in the initiation of humoral immunity in chickens.
The presence of neuroendocrine immune interaction in mammalian species has been studied extensively and has been established. However, such an interaction is not as well established in avian species. Furthermore, the role of such an interaction in the initiation of humoral immunity is not well understood. Therefore, the present studies were conducted to determine mechanisms involved in the initiation of humoral immunity in chickens. Cornell K-strain White Leghorn immature male chickens were used for all the experiments. Changes in hormonal and leukocyte profiles after antigen stimulation were studied. The ability of different leukocytes to produce ACTH was also investigated. It was concluded that the first step in the initiation of humoral immunity after antigen exposure is the release of interleukin-1 by macrophages, which in turn stimulates the production of CRF by hypothalamus and/or leukocytes. It is important to mention that CRF production could also be a direct effect of antigen stimulation. The CRF will then stimulate ACTH production by anterior pituitary and/or leukocytes. In addition, CRF will directly enhance lymphocyte activities in the spleen. Corticosteroid production will be stimulated by ACTH and will cause redistribution of lymphocytes from circulation to secondary lymphoid organs such as the spleen for antigen processing and eventual production of antibodies against the invading antigens. Finally, both ACTH and corticosteroids will later act in a negative feedback manner to regulate and control the process of antibody production by inhibiting lymphocyte activities and/or reducing the responsiveness to different stimuli.
Mashaly
M M
MM
Department of Poultry Science, Pennsylvania State University, University Park 16802, USA.
Trout
J M
JM
Hendricks
G
G
al-Dokhi
L M
LM
Gehad
A
A
D000324:Adrenocorticotropic Hormone / Q000096:biosynthesis / Q000097:blood / Q000276:immunology; D000818:Animals; D000917:Antibody Formation / Q000276:immunology* / Q000502:physiology; D000942:Antigens, Bacterial / Q000276:immunology; D002003:Brucella abortus / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000737:chemistry / Q000276:immunology; D002645:Chickens / Q000276:immunology* / Q000502:physiology; D003345:Corticosterone / Q000096:biosynthesis / Q000097:blood / Q000276:immunology; D003346:Corticotropin-Releasing Hormone / Q000276:immunology / Q000494:pharmacology; D005246:Feedback; D005260:Female; D007962:Leukocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008297:Male; D015213:Neuroimmunomodulation / Q000276:immunology* / Q000502:physiology; D009490:Neurosecretory Systems / Q000276:immunology* / Q000502:physiology; D012475:Salmonella / Q000276:immunology; D014284:Triiodothyronine / Q000096:biosynthesis / Q000097:blood / Q000276:immunology
D000942:Antigens, Bacterial; D014284:Triiodothyronine; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone