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Role of bacteria in the etiopathogenesis of inflammatory bowel disease

机译:细菌在炎症性肠病的发病机制中的作用

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摘要

Increased numbers of mucosa-associated Escherichia coli are observed in both of the major inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC). A potential pathophysiological link between the presence of pathogenic invasive bacteria and genetic host susceptibility of patients with ileal CD is suspected. In CD patients, with increased ileal expression of the CEACAM6 molecule acting as a receptor recognized by type 1 pilus bacterial adhesin, and with the identification of mutations in the NOD2-encoding gene, the presence of pathogenic invasive bacteria could be the link between abnormal ileal bacterial colonization and innate immune responses to invasive bacteria. In a susceptible host, the sequential etiological steps of the disease induced by adherent-invasive E. coli (AIEC) are: (1) abnormal colonization via binding to the CEACAM6 receptor, which is overexpressed in the ileal mucosa of CD patients; (2) ability to adhere to and to invade intestinal epithelial cells, which allows bacteria to cross the mucosal barrier; (3) survival and replication within infected macrophages in the lamina propria; and (4) induction of tumor necrosis factor-α secretion and granuloma formation.
机译:在主要的炎症性肠病,克罗恩病(CD)和溃疡性结肠炎(UC)中都观察到与粘膜相关的大肠杆菌数量增加。怀疑回肠CD患者的病原性入侵细菌的存在与遗传宿主易感性之间的潜在病理生理联系。在CD患者中,随着CEACAM6分子作为1型菌毛细菌粘附素识别的受体的回肠表达增加,并且鉴定到NOD2编码基因中的突变,致病性侵染细菌的存在可能是异常回肠之间的联系细菌定植和对入侵细菌的先天免疫反应。在易感宿主中,由粘附侵袭性大肠杆菌(AIEC)诱发的疾病的顺序病因学步骤是:(1)通过与CEACAM6受体结合而异常定植,在CD患者的回肠粘膜中过表达; (2)粘附和侵袭肠上皮细胞的能力,使细菌能够穿过粘膜屏障; (3)固有层感染巨噬细胞内的存活和复制; (4)诱导肿瘤坏死因子-α分泌和肉芽肿形成。

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