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Antigenic role of stress-induced catalase of Salmonella typhimurium in cell-mediated immunity.

机译:应激诱导鼠伤寒沙门氏菌过氧化氢酶在细胞介导的免疫中的抗原作用。

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摘要

The ability of the H2O2-induced catalase of Salmonella typhimurium to induce cell-mediated immunity against S. typhimurium infection in mice was examined. When exponentially growing cells of S. typhimurium were treated with 20 microM H2O2, the cells resisted killing by 1 mM H2O2 and showed the induction of a new species of catalase in addition to the constitutively produced one. Two molecules of catalases in S. typhimurium were isolated from mutant strains: H2O2-induced catalase (catalase II, 320 kDa), from a regulatory gene-deficient oxyR1 mutant, and constitutive catalase (catalase I, 350 kDa), from a katG gene-deleted mutant. When mice were inoculated with a sublethal dose of live cells, an intensive protective immunity (100% survival at 3 weeks) after challenge with a virulent strain associated with the delayed-type footpad hypersensitivity (DTH) reactions to both catalase I and catalase II was induced. Conversely, mice immunized with formalin-killed virulent S. typhimurium did not elicit protective immunity or DTH to either catalase. When mice were immunized with catalase I or catalase II, an enhanced protection (to a certain extent: 50% survival at 3 weeks) was induced in mice immunized with catalase II associated with DTH which did not cross-react with catalase I but not in those given catalase I. These results suggest that H2O2-induced stress proteins, including catalase II, are the dominant antigens for cell-mediated immunity in live cells of S. typhimurium and that a burst of such stress proteins in live salmonellae in phagocytes is responsible for the induction of cell-mediated immunity that is largely involved in the protection of susceptible mice against Salmonella infection.
机译:检查了H2O2诱导的鼠伤寒沙门氏菌过氧化氢酶诱导小鼠介导的针对鼠伤寒沙门氏菌感染的免疫力。当用20 microM H2O2处理鼠伤寒沙门氏菌的指数生长细胞时,这些细胞抵抗1 mM H2O2的杀伤作用,除组成性产生的一种过氧化氢酶外,还诱导了另一种过氧化氢酶的诱导。从突变菌株中分离到鼠伤寒沙门氏菌中的两个过氧化氢酶分子:H2O2诱导的过氧化氢酶(过氧化氢酶II,320 kDa),从调控基因缺陷的oxyR1突变体中分离;以及组成型过氧化氢酶(过氧化氢酶I,350 kDa),来自katG基因。缺失的突变体。当给小鼠接种亚致死剂量的活细胞时,用与对过氧化氢酶I和过氧化氢酶II的延迟型脚垫超敏性(DTH)反应相关的强毒株攻击后,即可获得增强的保护性免疫(3周存活率100%)。诱导的。相反,用福尔马林杀伤力强的鼠伤寒沙门氏菌免疫的小鼠未引起对两种过氧化氢酶的保护性免疫或DTH。当用过氧化氢酶I或过氧化氢酶II免疫小鼠时,在与DTH相关的过氧化氢酶II免疫的小鼠中诱导了增强的保护作用(在一定程度上:3周存活率达50%),而过氧化氢酶I与过氧化氢酶I没有交叉反应,但在这些结果表明,H2O2诱导的应激蛋白(包括过氧化氢酶II)是鼠伤寒沙门氏菌活细胞中细胞介导的免疫力的主要抗原,吞噬细胞中活沙门氏菌中此类应激蛋白的爆发是造成这种情况的原因。诱导细胞介导的免疫反应,在很大程度上保护了易感小鼠免受沙门氏菌感染。

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