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首页> 外文期刊>Infection and immunity >Regulatory Effects of Macrophage Inflammatory Protein 1α/CCL3 on the Development of Immunity to Cryptococcus neoformans Depend on Expression of Early Inflammatory Cytokines
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Regulatory Effects of Macrophage Inflammatory Protein 1α/CCL3 on the Development of Immunity to Cryptococcus neoformans Depend on Expression of Early Inflammatory Cytokines

机译：巨噬细胞炎性蛋白1α/ CCL3对新型隐球菌免疫发育的调节作用取决于早期炎性细胞因子的表达

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Macrophage inflammatory protein 1α (MIP-1α)/CCL3 prevents the development of eosinophilic pneumonia (EP) driven by a nonprotective T2-type immunity during infection with a highly virulent strain ofCryptococcus neoformans. The present study evaluated the interaction of MIP-1α with other innate immune system cytokines by comparing the immune responses that followed pulmonary infections with high- (C. neoformans 145A) and low (C. neoformans 52D)-virulence strains. In contrast to what was found for C. neoformans 145A infection, lack of MIP-1α in C. neoformans 52D infection did not cause the development of EP. C. neoformans 52D induced tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), and MCP-1 in the lungs of infected wild-type (WT) and MIP-1α knockout (KO) mice by day 7 postinfection. Both WT and MIP-1α KO mice subsequently cleared this infection. Thus, the robust expression of early inflammatory cytokines in C. neoformans 52D-infected mice promoted the development of protective immunity even in the absence of MIP-1α. Alternatively, C. neoformans145A-infected WT and MIP-1α KO mice had diminished TNF-α, IFN-γ, and macrophage chemoattractant protein 1 (MCP-1) responses, indicating that virulent C. neoformans 145A evaded early innate host defenses. However C. neoformans145A-infected WT mice had an early induction of MIP-1α and subsequently did not develop EP. In contrast, C. neoformans 145A-infected MIP-1α KO mice developed EP and had increased C. neoformans dissemination into the brain by day 35. We conclude that, in the absence of other innate immune response effector molecules, MIP-1α is crucial to prevent the development of EP and to control C. neoformansdissemination to the brain.
机译：巨噬细胞炎性蛋白1α（MIP-1α）/ CCL3可防止感染高致病性新型隐球菌的非保护性T2型免疫引起的嗜酸性肺炎（EP）的发展。本研究通过比较高（ C。newformans 145A）和低（ C。neoformans）肺部感染后的免疫应答，评估了MIP-1α与其他先天免疫系统细胞因子的相互作用。 52D）毒力菌株。与 C发现的相反。新甲虫 145A感染， C中缺少MIP-1α。新甲虫52D感染并未引起EP的发展。 C。新形成的52D诱导野生型（WT）和MIP-1α基因敲除（KO）小鼠肺部肿瘤坏死因子α（TNF-α），γ干扰素（IFN-γ）和MCP-1感染后第7天。 WT和MIP-1αKO小鼠随后均清除了这种感染。因此，早期炎症细胞因子在 C中的强烈表达。即使没有MIP-1α，感染52D的新福尔摩斯小鼠也能促进保护性免疫的发展。或者， C。感染新甲虫145A的WT和MIP-1αKO小鼠的TNF-α，IFN-γ和巨噬细胞趋化蛋白1（MCP-1）应答减弱，表明有毒的 C。新甲虫145A躲避了早期的先天防御。但是 C。感染新福尔摩斯 145A的WT小鼠具有MIP-1α的早期诱导能力，随后未发育成EP。相反， C。感染145A​​的新甲虫感染MIP-1αKO小鼠出现EP，并增加 C。到35天时，新甲虫便会散布到大脑中。我们的结论是，在没有其他先天性免疫应答效应分子的情况下，MIP-1α对于预防EP的发展和控制 C至关重要。新甲虫传播到大脑。

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