Department of Physiology and Pharmacology, Inflammation Research Network and Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta, Canada.
Am J Physiol Gastrointest Liver Physiol. 2022 Jan 1;322(1):G169-G182. doi: 10.1152/ajpgi.00194.2021. Epub 2021 Dec 8.
Mucosal and histological healing have become the gold standards for assessing the efficacy of therapy in patients living with inflammatory bowel diseases (IBD). Despite these being the accepted goals in therapy, the mechanisms that underlie the healing of the mucosa after an inflammatory insult are not well understood, and many patients fail to meet this therapeutic endpoint. Here we review the emerging evidence that mediators (e.g., prostaglandins, cytokines, proteases, reactive oxygen, and nitrogen species) and innate immune cells (e.g., neutrophils and monocytes/macrophages), that are involved in the initiation of the inflammatory response, are also key players in the mechanisms underlying mucosal healing to resolve chronic inflammation in the colon. The dual function mediators comprise an inflammation/repair program that returns damaged tissue to homeostasis. Understanding details of the dual mechanisms of these mediators and cells may provide the basis for the development of drugs that can help to stimulate epithelial repair in patients affected by IBD.
黏膜和组织学愈合已成为评估炎症性肠病 (IBD) 患者治疗效果的金标准。尽管这些是治疗的公认目标，但在炎症损伤后黏膜愈合的机制尚不清楚，许多患者未能达到这一治疗终点。在这里，我们回顾了一些新出现的证据，表明参与炎症反应启动的介质（例如前列腺素、细胞因子、蛋白酶、活性氧和氮物种）和固有免疫细胞（例如中性粒细胞和单核细胞/巨噬细胞）也是黏膜愈合机制中的关键因素，以解决结肠中的慢性炎症。双重功能介质构成了一个炎症/修复程序，将受损组织恢复到体内平衡。了解这些介质和细胞双重机制的细节可能为开发药物提供基础，这些药物可以帮助刺激受 IBD 影响的患者的上皮修复。
