Mashaly M M, Trout J M, Hendricks G, al-Dokhi L M, Gehad A
Department of Poultry Science, Pennsylvania State University, University Park 16802, USA.
Domest Anim Endocrinol. 1998 Sep;15(5):409-22. doi: 10.1016/s0739-7240(98)00023-x.
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.
哺乳动物中神经内分泌免疫相互作用的存在已得到广泛研究并得以确立。然而,这种相互作用在禽类中尚未得到充分证实。此外,这种相互作用在体液免疫启动中的作用也尚未完全了解。因此,本研究旨在确定鸡体液免疫启动所涉及的机制。所有实验均使用康奈尔K系白来航未成熟雄性鸡。研究了抗原刺激后激素和白细胞谱的变化。还研究了不同白细胞产生促肾上腺皮质激素(ACTH)的能力。得出的结论是,抗原暴露后体液免疫启动的第一步是巨噬细胞释放白细胞介素-1,进而刺激下丘脑和/或白细胞产生促肾上腺皮质激素释放因子(CRF)。需要指出的是,CRF的产生也可能是抗原刺激的直接作用。然后,CRF将刺激垂体前叶和/或白细胞产生ACTH。此外,CRF将直接增强脾脏中的淋巴细胞活性。促肾上腺皮质激素将刺激皮质类固醇的产生,并导致淋巴细胞从循环系统重新分布到脾脏等二级淋巴器官,以进行抗原处理并最终产生针对入侵抗原的抗体。最后,ACTH和皮质类固醇随后将以负反馈方式发挥作用,通过抑制淋巴细胞活性和/或降低对不同刺激的反应性来调节和控制抗体产生过程。