Studies on the neuro-endocrine regulatory mechanism for mucosal immune system

有大量的证据表明，神经激素对胃肠道粘膜免疫炎症反应的各个方面都有影响。肠道包含高度专门化的神经内分泌和免疫系统，粘膜表面经过精心设计，允许神经和免疫系统细胞之间的相互作用。肠黏膜中含有大量的神经肽和神经递质，如血管活性肠肽（VIP）、P物质（SP）和生长抑素（SOM）等，它们调节肠黏膜中包括肠相关淋巴组织（GALT）在内的免疫效应细胞的功能。在正常肠黏膜中，含神经肽的神经与腺体、血管和免疫效应细胞密切相关，VIP和SP仅存在于神经中，VIP mRNA存在于部分内分泌细胞和巨噬细胞中。在溃疡性结肠炎（UC）粘膜中，沿增生和扩张的小静脉样血管可见VIP-和SP-神经的神经支配增加，这些神经强烈表达多种细胞粘附分子，包括ICAM-1（CD54）和e-选择素。隐窝脓肿周围的神经几乎不存在。这些含神经肽神经的分布异常可能干扰UC粘膜的免疫炎症调节，引起粘膜损伤。肠黏膜免疫细胞上的神经肽受体进一步证明了神经与粘膜免疫系统之间可能存在功能性相互作用。B细胞系和t细胞系的淋巴细胞均可表达神经肽受体，而在粘膜免疫系统成熟之前，新生儿的皮耶氏斑生发中心（FDC）的树突状细胞和固有层的巨噬细胞也携带这些受体。神经内分泌-免疫相互作用的异常和不成熟可能在肠道免疫炎性疾病的发病机制中起重要作用，并导致粘膜损伤和延长炎症。心理压力可以通过神经内分泌-免疫相互关系影响炎症性肠病的症状。少

There is a great deal of evidence for the neurohormonal influence on vasious aspects of the immuno-inflammatory response of the gastrointestinal mucosa. The intestine contains highly specialized subdivision of both the neuroendocrine and immune systems, and the mucosal surface is specially well designed to allow for interactions between nerves and the cells of the immune system. The intestinal mucosa contains significant amount of the neuropeptide, neurotransmitters, such as vasoactive intestinal peptide (VIP), substance P (SP) and somatostatin (SOM), which have been shown to regulate the function of immune effector cells including gut-associated lymphoid tissue (GALT) in the intestinal mucosa.In normal intestinal mucosa neuropeptide-containing nerves are intimately correlated to glands, blood vessels, and immune effector cells, VIP and SP are solely present in nerves, and mRNA for VIP found in a part of endocrine cells and macrophages. In hypervascular areas with active inflammation i … More n the ulcerative colitis (UC) mucosa, increasing innervation of VIP- and SP- nerves are observed along the proliferated and dilated venule-like blood vessels, which strongly express several cell adhesion molecules including ICAM-1(CD54) and E-selectin. These nerves around crypt abscess were almost absent. These distribution abnormalities of neuropeptide-containing nerves may disturb the immuno-inflammatory regulation in the UC mucosa, and cause the mucosal damage.Neuropeptide recepters on immunocytes in the intestinal mucosa have added further evidence to the notion that functional interaction between nerves and mucosal immune system can exist. Lymphocytes of both B- and T-cell lineages can express neuropeptide recepter, and dendritic cells of the germinal center of Peyer's patches (FDC) and macrophages in the lamina propria also carry these receptors, which are absent in FDC of neonates before the mucosal immune system matures.Abnormalities and immaturity in the neuroendocrine-immune interactions may be important in the desease pathogenesis in immuno-inflammatory disorders in the intestine, and cause the mucosal damage and prolonged inflammation. Psychological stress can influence the symptoms of inflammatory bowel disease through the neuroendocrine-immune interrelationship. Less