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首页> 外文期刊>Infection and immunity >Caspase-1 Mediates Resistance in Murine Melioidosis
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Caspase-1 Mediates Resistance in Murine Melioidosis

机译：半胱氨酸天冬氨酸蛋白酶1介导耐药性在小鼠类神经病

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The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell to cell. Recently, it has been shown that B. pseudomallei can induce caspase-1-dependent cell death in macrophages. The aim of the present study was to further elucidate the role of caspase-1 during B. pseudomallei infection. In vivo experiments with caspase-1?/? mice revealed a high susceptibility to B. pseudomallei challenge. This phenotype was associated with a significantly higher bacterial burden 2 days after infection and decreased gamma interferon (IFN-γ) and interleukin-18 cytokine levels 24 h after infection compared to control animals. caspase-1?/? bone marrow-derived macrophages (BMM) exhibited strong caspase-3 expression and reduced cell damage compared to wild-type (WT) cells during early B. pseudomallei infection, indicating “classical” apoptosis, whereas WT BMM showed signs of rapid caspase-1-dependent cell death. Moreover, we found that caspase-1?/? BMM had a strongly increased bacterial burden compared to WT cells 3 h after infection under conditions where no difference in cell death could be observed between both cell populations at this time point. We therefore suggest that caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for B. pseudomallei, but, in addition, caspase-1 might also have a role in controlling intracellular replication of B. pseudomallei in macrophages. Moreover, caspase-1-dependent IFN-γ production is likely to contribute to resistance in murine melioidosis.
机译：革兰氏阴性杆菌伯克霍尔德菌假mallei 是类鼻oid病的病原体，类li尾病是一种潜在的致命疾病，在热带和亚热带地区流行。细菌在细胞质内在细胞内繁殖，诱导肌动蛋白尾巴的形成，并可以直接在细胞之间传播。最近，已显示 B。假Mallei 可以诱导巨噬细胞中caspase-1依赖性细胞死亡。本研究的目的是进一步阐明caspase-1在 B期间的作用。假小肠感染。对 caspase-1 ？/？小鼠进行的体内实验显示，其对 B的敏感性很高。假小麦挑战。与对照动物相比，该表型与感染后2天的细菌负荷显着增加以及感染后24 hγ干扰素（IFN-γ）和白介素18细胞因子水平降低有关。与早期野生型（WT）细胞相比， caspase-1 ？/？骨髓源性巨噬细胞（BMM）与野生型（WT）细胞相比，具有较强的caspase-3表达并减少了细胞损伤。 em> B。假性小肠感染，表明“经典”细胞凋亡，而野生型BMM显示出快速的caspase-1依赖性细胞死亡迹象。此外，我们发现与感染后3 h的WT细胞相比， caspase-1 ？/？ BMM在细胞死亡无差异的条件下，其细菌负担大大增加。在这个时间点两个细胞群之间观察到。因此，我们建议依赖caspase-1的快速细胞死亡可能通过减少 B的细胞内利基而有助于抵抗。假单胞菌，但除此之外，caspase-1也可能在控制 B的细胞内复制中起作用。巨噬细胞中的假小麦芽。此外，caspase-1依赖的IFN-γ的产生很可能有助于鼠类me虫病的耐药性。

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