肠胶质细胞正在成为肠道运动调节的关键参与者,分泌,上皮屏障功能,以及健康和疾病中的肠道稳态。肠神经胶质细胞通过转化为“反应性神经胶质表型”和肠神经胶质增生对肠道炎症做出反应,导致神经炎症,肠神经病,肠运动障碍和运动障碍,腹泻或便秘,\'漏肠\',还有内脏疼痛.微型审查的重点是炎症对肠神经胶质反应性的影响,以应对各种侮辱,例如肠道手术,缺血,感染(C.艰难感染,HIV-Tat引起的腹泻,内毒素血症和麻痹性肠梗阻),胃肠道疾病(炎症性肠病,憩室病,坏死性小肠结肠炎,结直肠癌)和功能性胃肠道疾病(术后肠梗阻,慢性假性肠梗阻,便秘,肠易激综合征)。近年来在胶质反应性和肠胶质增生的分子致病机制方面取得了重大进展,导致肠神经病,运动中断,腹泻,内脏过敏和腹痛。越来越多的神经胶质分子靶标具有治疗意义,包括白细胞介素-1(IL-1R)的受体,嘌呤(P2X2R,A2BR),PPARα,溶血磷脂酸(LPAR1),Toll样受体4(TLR4R),雌激素-β受体(ERβ)肾上腺素能α-2(α-2R)和内皮素B(ETBR),连接蛋白-43/集落刺激因子1信号(Cx43/CSF1)和S100β/RAGE信号通路。这些令人兴奋的新发展是微型审查的主题。临床前模型中的一些发现可能是可以翻译给人类的,提高了设计未来临床试验以测试治疗应用的可能性。总的来说,对肠胶质细胞的研究在我们对胃肠道病理生理学的理解方面取得了重大进展。
Enteric glial cells are emerging as critical players in the regulation of intestinal motility, secretion, epithelial barrier function, and gut homeostasis in health and disease. Enteric glia react to intestinal inflammation by converting to a \'reactive glial phenotype\' and enteric gliosis, contributing to neuroinflammation, enteric neuropathy, bowel motor dysfunction and dysmotility, diarrhea or constipation, \'leaky gut\', and visceral pain. The focus of the minireview is on the impact of inflammation on enteric glia reactivity in response to diverse insults such as intestinal surgery, ischemia, infections (C. difficile infection, HIV-Tat-induced diarrhea, endotoxemia and paralytic ileus), GI diseases (inflammatory bowel diseases, diverticular disease, necrotizing enterocolitis, colorectal cancer) and functional GI disorders (postoperative ileus, chronic intestinal pseudo-obstruction, constipation, irritable bowel syndrome). Significant progress has been made in recent years on molecular pathogenic mechanisms of glial reactivity and enteric gliosis, resulting in enteric neuropathy, disruption of motility, diarrhea, visceral hypersensitivity and abdominal pain. There is a growing number of glial molecular targets with therapeutic implications that includes receptors for interleukin-1 (IL-1R), purines (P2X2R, A2BR), PPARα, lysophosphatidic acid (LPAR1), Toll-like receptor 4 (TLR4R), estrogen-β receptor (ERβ) adrenergic α-2 (α-2R) and endothelin B (ETBR), connexin-43 / Colony-stimulating factor 1 signaling (Cx43/CSF1) and the S100β/RAGE signaling pathway. These exciting new developments are the subject of the minireview. Some of the findings in pre-clinical models may be translatable to humans, raising the possibility of designing future clinical trials to test therapeutic application(s). Overall, research on enteric glia has resulted in significant advances in our understanding of GI pathophysiology.