急性腹膜炎G.V. Bulava发病的免疫机制

G. V. Bulava
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引用次数: 0

摘要

腹膜的急性炎症-腹膜炎-通常发生在内脏器官损伤、肠坏死、吻合失败或肿瘤发生后。随后腹腔的微生物污染导致感染,免疫机制因此被激活。腹腔炎症过程的发病机制及其特征在很大程度上取决于腹膜的结构和功能,以及腹膜与网膜的密切联系。解决腹膜炎的一个重要问题是维持细胞因子的平衡,免疫细胞的活性和补体功能在腹膜和网膜的免疫淋巴簇,以及它们在炎症期间的协同作用。本文综述了腹膜和网膜的结构和功能、中性粒细胞、巨噬细胞、免疫系统淋巴细胞环节以及促炎性和抗炎性细胞因子和补体在腹腔急性炎症的发生和停止中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Immune mechanisms in the pathogenesis of acute peritonitis G.V. Bulava
Acute inflammation of the peritoneum – peritonitis – often develops after injury to hollow visceral organs, intestinal necrosis, failure of anastomosis, or tumor processes. Subsequent microbial contamination of the abdominal cavity leads to infection, in response to which immune mechanisms are activated. The pathogenesis of inflammatory processes in the abdominal cavity and their features are largely determined by the structure and function of the peritoneum, as well as its close connection with the omentum. An important point in resolving peritonitis is to maintain the balance of cytokines, the activity of immunocytes and complement functioning in the immune lymphoid clusters of the peritoneum and omentum, and their collaborative action during inflammation. The review presents data on the structure and function of the peritoneum and omentum, the role of neutrophil, macrophage, lymphocytic links of the immune system, as well as those of pro- and anti-inflammatory cytokines and complement in the development and cessation of acute inflammation in the abdominal cavity.
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