Farncombe Family Digestive Health Research Institute, Department of Pathology and Molecular Medicine, McMaster University, ON, Canada.
Clin Exp Immunol. 2010 Jul 1;161(1):19-27. doi: 10.1111/j.1365-2249.2010.04150.x. Epub 2010 Apr 9.
Gut inflammation is characterized by mucosal recruitment of activated cells from both the innate and adaptive immune systems. In addition to immune cells, inflammation in the gut is associated with an alteration in enteric endocrine cells and various biologically active compounds produced by these cells. Although the change in enteric endocrine cells or their products is considered to be important in regulating gut physiology (motility and secretion), it is not clear whether the change plays any role in immune activation and in the regulation of gut inflammation. Due to the strategic location of enteric endocrine cells in gut mucosa, these gut hormones may play an important role in immune activation and promotion of inflammation in the gut. This review addresses the research on the interface between immune and endocrine systems in gastrointestinal (GI) pathophysiology, specifically in the context of two major products of enteric endocrine systems, namely serotonin (5-hydroxytryptamine: 5-HT) and chromogranins (Cgs), in relation to immune activation and generation of inflammation. The studies reviewed in this paper demonstrate that 5-HT activates the immune cells to produce proinflammatory mediators and by manipulating the 5-HT system it is possible to modulate gut inflammation. In the case of Cgs the scenario is more complex, as this hormone has been shown to play both proinflammatory and anti-inflammatory functions. It is also possible that interaction between 5-HT and Cgs may play a role in the modulation of immune and inflammatory responses. In addition to enhancing our understanding of immunoendocrine interaction in the gut, the data generated from the these studies may have implications in understanding the role of gut hormone in the pathogenesis of both GI and non-GI inflammatory diseases which may lead ultimately to improved therapeutic strategies in inflammatory disorders.
肠道炎症的特征是固有免疫和适应性免疫系统的激活细胞募集到黏膜。除了免疫细胞外,肠道炎症还与肠内分泌细胞的改变以及这些细胞产生的各种生物活性化合物有关。尽管肠内分泌细胞或其产物的变化被认为在调节肠道生理(蠕动和分泌)方面很重要,但尚不清楚这种变化是否在免疫激活和肠道炎症的调节中发挥作用。由于肠内分泌细胞在肠道黏膜中的位置很重要,这些肠道激素可能在免疫激活和促进肠道炎症中发挥重要作用。这篇综述探讨了胃肠道(GI)病理生理学中免疫系统和内分泌系统之间的相互作用,特别是涉及肠内分泌系统的两个主要产物,即 5-羟色胺(5-HT)和嗜铬粒蛋白(Cgs),与免疫激活和炎症发生的关系。本文综述的研究表明,5-HT 可激活免疫细胞产生促炎介质,通过操纵 5-HT 系统,可以调节肠道炎症。在 Cgs 的情况下,情况更为复杂,因为已经表明这种激素具有促炎和抗炎作用。5-HT 和 Cgs 之间的相互作用也可能在调节免疫和炎症反应中发挥作用。除了增强我们对肠道中免疫内分泌相互作用的理解外,这些研究产生的数据可能对理解肠道激素在 GI 和非 GI 炎症性疾病发病机制中的作用具有重要意义,最终可能导致炎症性疾病治疗策略的改善。