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Induction of mucosal immune responses by bacteria and bacterial components

机译:细菌和细菌成分诱导粘膜免疫反应

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摘要

Bacteria have well documented abilities to induce protective as well as pathogenic mucosal immune responses, with the type of response dependent on the genetically programmed balance of pro- and anti-inflammatory cytokines and T-lymphocyte subsets. Inflammatory bowel disease, especially Crohn disease and periodontal disease, appear to be overly aggressive cellular immune responses to some, but not all, normal resident bacteria. Recent evidence suggests that the balance of protective (probiotic) and aggressive commensal luminal bacterial species is an additional determinant of mucosal homeostasis (tolerance) versus pathogenic immune responses (loss of tolerance) and that this balance can be therapeutically manipulated. Mucosal pathogens elicit a characteristic profile of cytokines from epithelial cells, including chemokines that recruit effector cells to the site of invasion to clear the invading organism. The molecular mechanisms of epithelial attachment and invasion of bacterial pathogens (eg, Salmonella, Shigella, pathogenic Escherichia coli, and Yersinia) and the mechanisms of injury induced by Clostridium difficile toxins and Helicobacter pylori are beginning to be understood, as are the innate and cognate host immune responses to these organisms, leading to novel means to effectively block bacterial injury and induce protective immune responses through immunization.
机译:细菌具有诱导保护性和致病性粘膜免疫反应的能力,文献记载的能力取决于反应性和抗炎性细胞因子和T淋巴细胞亚群的基因编程平衡。炎性肠病,尤其是克罗恩病和牙周病,似乎是对某些而非全部正常常驻细菌的过度攻击性细胞免疫反应。最近的证据表明,保护性(益生菌)和侵略性共生腔细菌物种之间的平衡是粘膜稳态(耐受性)与病原性免疫反应(耐受性丧失)的另一个决定因素,并且这种平衡可以通过治疗来控制。粘膜病原体从上皮细胞引起细胞因子的特征性分布,包括趋化因子将趋化因子细胞募集到入侵部位以清除入侵生物。细菌病原体(例如沙门氏菌,志贺氏菌,致病性大肠杆菌和耶尔森氏菌)的上皮附着和侵袭的分子机制以及难辨梭状芽孢杆菌毒素和幽门螺杆菌引起的损伤机制已被理解,先天和同源宿主对这些生物体的免疫反应,从而导致有效地阻止细菌损伤并通过免疫诱导保护性免疫反应的新手段。

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