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Activated intestinal macrophages in patients with cirrhosis release NO and IL-6 that may disrupt intestinal barrier function

机译:肝硬化患者激活的肠巨噬细胞释放NO和IL-6,可能会破坏肠屏障功能

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摘要

Bacterial infections commonly complicate decom-pensated cirrhosis and are thought to be associated with increased bacterial translocation across the intestinal barrier (Gastroenterology 2011;141:1220-1230; Hepatology 2006;44:633-639). Alterations in circulating bacterial DNA, even in the presence of negative cultures, increases the risk of hepatic decompensation, variceal hemorrhage, and hep-atorenal syndrome (Gastroenterology 2007; 133: 818-824). In health, the gut epithelial barrier provides an effective barrier against microorganisms while simultaneously providing a semipermeable membrane for nutrient absorption (Nat Rev Immunol 2009;9:799-809). In cirrhosis, studies have confirmed that intestinal bacterial flora is altered (Hepatology 2006;45:744-757). However, it is unclear why the intestinal epithelial barrier fails, facilitating translocation of bacterial products and DNA (Hepatology 2008;48:1924-1931; Hepatology 2010;52:2044-2052).
机译:细菌感染通常使分解性肝硬化复杂化,并被认为与细菌通过肠道屏障的转运增加有关(Gastroenterology 2011; 141:1220-1230; Hepatology 2006; 44:633-639)。即使存在阴性培养物,循环细菌DNA的改变也会增加肝代偿失调,静脉曲张破裂出血和肝肾上腺综合征的风险(Gastroenterology 2007; 133:818-824)。在健康方面,肠道上皮屏障可有效抵抗微生物,同时提供半透膜以吸收营养(Nat Rev Immunol 2009; 9:799-809)。在肝硬化中,研究已证实肠道细菌菌群发生了变化(Hepatology 2006; 45:744-757)。然而,尚不清楚为什么肠上皮屏障失效,从而促进细菌产物和DNA的易位(Hepatology 2008; 48:1924-1931; Hepatology 2010; 52:2044-2052)。

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