Aggarwal Surbhi, Ranjha Raju, Paul Jaishree
Department of Biochemical Engineering and Biotechnology, Indian Institute of Technology, Delhi 110016, India.
School of Life Sciences, Jawaharlal Nehru University, Delhi 110067, India.
World J Gastrointest Pathophysiol. 2021 May 22;12(3):25-39. doi: 10.4291/wjgp.v12.i3.25.
Microbes colonize the gastrointestinal tract are considered as highest complex ecosystem because of having diverse bacterial species and 150 times more genes as compared to the human genome. Imbalance or dysbiosis in gut bacteria can cause dysregulation in gut homeostasis that subsequently activates the immune system, which leads to the development of inflammatory bowel disease (IBD). Neuromediators, including both neurotransmitters and neuropeptides, may contribute to the development of aberrant immune response. They are emerging as a regulator of inflammatory processes and play a key role in various autoimmune and inflammatory diseases. Neuromediators may influence immune cell's function the receptors present on these cells. The cytokines secreted by the immune cells, in turn, regulate the neuronal functions by binding with their receptors present on sensory neurons. This bidirectional communication of the enteric nervous system and the enteric immune system is involved in regulating the magnitude of inflammatory pathways. Alterations in gut bacteria influence the level of neuromediators in the colon, which may affect the gastrointestinal inflammation in a disease condition. Changed neuromediators concentration dysbiosis in gut microbiota is one of the novel approaches to understand the pathogenesis of IBD. In this article, we reviewed the existing knowledge on the role of neuromediators governing the pathogenesis of IBD, focusing on the reciprocal relationship among the gut microbiota, neuromediators, and host immunity. Understanding the neuromediators and host-microbiota interactions would give a better insight in to the disease pathophysiology and help in developing the new therapeutic approaches for the disease.
定居在胃肠道的微生物被认为是高度复杂的生态系统，因为其具有多样的细菌种类，且基因数量是人类基因组的150倍之多。肠道细菌的失衡或失调会导致肠道内稳态的失调，进而激活免疫系统，引发炎症性肠病（IBD）。神经介质，包括神经递质和神经肽，可能促成异常免疫反应的发生。它们正成为炎症过程的调节因子，并在各种自身免疫性和炎症性疾病中发挥关键作用。神经介质可能通过这些细胞上存在的受体影响免疫细胞的功能。反过来，免疫细胞分泌的细胞因子通过与感觉神经元上存在的受体结合来调节神经元功能。肠神经系统和肠免疫系统的这种双向通信参与调节炎症途径的程度。肠道细菌的改变会影响结肠中神经介质的水平，这可能在疾病状态下影响胃肠道炎症。肠道微生物群中神经介质浓度的改变和失调是理解IBD发病机制的新方法之一。在本文中，我们回顾了关于神经介质在IBD发病机制中作用的现有知识，重点关注肠道微生物群、神经介质和宿主免疫之间的相互关系。了解神经介质与宿主-微生物群的相互作用将有助于更好地洞察疾病病理生理学，并有助于开发该疾病的新治疗方法。
