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首页> 外文期刊>Journal of gastroenterology and hepatology >Helicobacter pylori infection: mechanism of colonization and functional dyspepsia Reduced colonization of gastric mucosa by Helicobacter pylori in mice deficient in interleukin-10.
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Helicobacter pylori infection: mechanism of colonization and functional dyspepsia Reduced colonization of gastric mucosa by Helicobacter pylori in mice deficient in interleukin-10.

机译：幽门螺杆菌感染：定植和功能性消化不良的机制幽门螺杆菌在缺乏白介素10的小鼠中减少了胃粘膜的定植。

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BACKGROUND AND AIMS: Interleukin-10 (IL-10) is a potent anti-inflammatory and immunoregulatory cytokine. Mice deficient in IL-10 production (IL-10-/-mice) develop a spontaneous chronic enterocolitis, suggesting that IL-10 is an important regulator of the mucosal immune response in vivo. The objective of this study was to determine the role of endogenous IL-10 in the host defense against gastric colonization by Helicobacter pylori by using IL-10-deficient mice. METHODS: The IL-10-/-mice were inoculated intragastrically with a mouse-adapted H. pylori isolate (Sydney Strain 1). Gastric colonization by H. pylori (biopsy urease test and bacterial colony counts), serum levels of H. pylori-specific immunoglobulin (Ig) M, A, G, isotypes of IgG, and the gastric mucosal inflammatory scores were determined 6 weeks after inoculation. Results were compared with those obtained from H. pylori-infected control mice (IL-10+/-mice). RESULTS: The colonization of gastric mucosa by H. pylori was reduced approximately 100-fold (P < 0.0001) in IL-10-/-mice (log10 4.87 +/- 0.26CFU/g tissue) as compared to IL-10+/-mice (log10 6.64 +/- 0.22 CFU/g tissue). Furthermore, IL-10-/-mice infected with H. pylori had significantly higher H. pylori-specific IgA and IgG antibodies in serum (P < or = 0.01), and developed much more severe chronic active gastritis than infected IL-10+/-mice. The median scores of the infiltration of gastric mucosa by mononuclear cells and neutrophils were up to threefold higher in IL-10-/-mice than they were in IL-10+/-mice. CONCLUSION: Our studies suggest that endogenous IL-10 is an inhibitor of the protective immune response to H. pylori infection. Interleukin-10 participates in the downregulation of H. pylori-induced gastric inflammatory responses, which apparently confers a survival advantage to the organism promoting more effective colonization of gastric mucosa.
机译：背景与目的：白介素-10（IL-10）是一种有效的抗炎和免疫调节细胞因子。缺乏IL-10产生的小鼠（IL-10-/-小鼠）会发展为自发性慢性小肠结肠炎，这表明IL-10是体内黏膜免疫反应的重要调节剂。这项研究的目的是确定内源性IL-10在宿主抵抗由幽门螺杆菌引起的幽门螺杆菌引起的胃定植中的作用，方法是使用IL-10缺陷小鼠。方法：用小鼠适应性幽门螺杆菌分离株（悉尼株1）在胃内接种IL-10-/-小鼠。在接种后6周确定幽门螺杆菌在胃中的定植（活检尿素酶测试和细菌菌落计数），幽门螺杆菌特异性免疫球蛋白（Ig）M，A，G，IgG同种型的血清水平以及胃黏膜炎性评分。将结果与从幽门螺杆菌感染的对照小鼠（IL-10 +/-小鼠）获得的结果进行比较。结果：与IL-10 + /相比，幽门螺杆菌在IL-10-/-小鼠（log10 4.87 +/- 0.26CFU / g组织）中对胃黏膜的定殖减少了约100倍（P <0.0001）。 -小鼠（log 10 6.64 +/- 0.22 CFU / g组织）。此外，感染幽门螺杆菌的IL-10-/-小鼠血清中的幽门螺杆菌特异性IgA和IgG抗体明显更高（P <或= 0.01），并且比感染的IL-10 +严重得多的慢性活动性胃炎/-老鼠。在IL-10-/-小鼠中，单核细胞和中性粒细胞浸润胃粘膜的中值比在IL-10 +/-中高三倍。结论：我们的研究表明内源性IL-10是抑制幽门螺杆菌感染的保护性免疫反应的抑制剂。白细胞介素10参与幽门螺杆菌诱导的胃炎症反应的下调，这显然赋予了生物以生存优势，从而促进了胃黏膜更有效的定殖。

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