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首页> 外文期刊>Infection and immunity >Caveolin-1-Deficient Mice Show Defects in Innate Immunity and Inflammatory Immune Response during Salmonella enterica Serovar Typhimurium Infection
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Caveolin-1-Deficient Mice Show Defects in Innate Immunity and Inflammatory Immune Response during Salmonella enterica Serovar Typhimurium Infection

机译：Caveolin-1缺陷小鼠在肠炎沙门氏菌血清鼠伤寒感染过程中显示出先天免疫和炎性免疫反应的缺陷。

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A number of studies have shown an association of pathogens with caveolae. To this date, however, there are no studies showing a role for caveolin-1 in modulating immune responses against pathogens. Interestingly, expression of caveolin-1 has been shown to occur in a regulated manner in immune cells in response to lipopolysaccharide (LPS). Here, we sought to determine the role of caveolin-1 (Cav-1) expression in Salmonella pathogenesis. Cav-1?/? mice displayed a significant decrease in survival when challenged with Salmonella enterica serovar Typhimurium. Spleen and tissue burdens were significantly higher in Cav-1?/? mice. However, infection of Cav-1?/? macrophages with serovar Typhimurium did not result in differences in bacterial invasion. In addition, Cav-1?/? mice displayed increased production of inflammatory cytokines, chemokines, and nitric oxide. Regardless of this, Cav-1?/? mice were unable to control the systemic infection of Salmonella. The increased chemokine production in Cav-1?/? mice resulted in greater infiltration of neutrophils into granulomas but did not alter the number of granulomas present. This was accompanied by increased necrosis in the liver. However, Cav-1?/? macrophages displayed increased inflammatory responses and increased nitric oxide production in vitro in response to Salmonella LPS. These results show that caveolin-1 plays a key role in regulating anti-inflammatory responses in macrophages. Taken together, these data suggest that the increased production of toxic mediators from macrophages lacking caveolin-1 is likely to be responsible for the marked susceptibility of caveolin-1-deficient mice to S. enterica serovar Typhimurium.
机译：大量研究表明，病原体与海绵体有关。然而，迄今为止，尚无研究表明小窝蛋白-1在调节针对病原体的免疫应答中的作用。有趣的是，已经证明小窝蛋白-1的表达在免疫细胞中响应脂多糖（LPS）以调节的方式发生。在这里，我们试图确定小窝蛋白1（Cav-1）表达在沙门氏菌发病机理中的作用。当感染沙门氏菌血清型鼠伤寒沙门氏菌时，Cav-1 ？/？小鼠的存活率显着降低。 Cav-1 ？/？小鼠的脾脏和组织负担明显更高。然而，鼠伤寒沙门氏菌感染Cav-1 ？/？巨噬细胞并没有导致细菌入侵的差异。此外，Cav-1 ？/？小鼠显示出炎症细胞因子，趋化因子和一氧化氮的产生增加。无论如何，Cav-1 ？/？小鼠无法控制沙门氏菌的全身感染。 Cav-1 α/β小鼠趋化因子产生的增加导致嗜中性粒细胞向肉芽肿中的浸润更大，但并未改变存在的肉芽肿的数量。这伴随着肝脏坏死的增加。然而，Cav-1 ？/？巨噬细胞在体外响应沙门氏菌 LPS表现出增强的炎症反应和一氧化氮生成。这些结果表明，caveolin-1在调节巨噬细胞的抗炎反应中起关键作用。综上所述，这些数据表明缺乏小窝蛋白1的巨噬细胞毒性介质的产生增加可能是小窝蛋白1缺陷小鼠对 S的明显易感性的原因。肠炎血清型鼠伤寒。

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