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首页> 外文期刊>Cellular microbiology >Anaplasma phagocytophilum surface protein AipA mediates invasion of mammalian host cells
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Anaplasma phagocytophilum surface protein AipA mediates invasion of mammalian host cells

机译：嗜浆细胞表面蛋白AipA介导哺乳动物宿主细胞的入侵

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摘要

Anaplasma phagocytophilum, which causes granulocytic anaplasmosis in humans and animals, is a tick-transmitted obligate intracellular bacterium that mediates its own uptake into neutrophils and non-phagocytic cells. Invasins of obligate intracellular pathogens are attractive targets for protecting against or curing infection because blocking the internalization step prevents survival of these organisms. The complement of A. phagocytophilum invasins is incompletely defined. Here, we report the significance of a novel A. phagocytophilum invasion protein, AipA. A. phagocytophilum induced aipA expression during transmission feeding of infected ticks on mice. The bacterium upregulated aipA transcription when it transitioned from its non-infectious reticulate cell morphotype to its infectious densecored morphotype during infection of HL-60 cells. AipA localized to the bacterial surface and was expressed during in vivo infection. Of the AipA regions predicted to be surface-exposed, only residues 1 to 87 (AipA_(1-87)) were found to be essential for host cell invasion. Recombinant AipA_(1-87) protein bound to and competitively inhibited A. phagocytophilum infection of mammalian cells. Antiserum specific for AipA_(1-87), but not other AipA regions, antagonized infection. Additional blocking experiments using peptide-specific antisera narrowed down the AipA invasion domain to residues 9 to 21. An antisera combination targeting AipA_(1-87) together with two other A. phagocytophilum invasins, OmpA and Asp14, nearly abolished infection of host cells. This study identifies AipA as an A. phagocytophilum surface protein that is critical for infection, demarcates its invasion domain, and establishes a rationale for targeting multiple invasins to protect against granulocytic anaplasmosis.
机译：吞噬性无浆细胞是导致人和动物的粒细胞性胞浆菌病的一种，是一种tick传播的专性细胞内细菌，介导自身吸收到嗜中性粒细胞和非吞噬细胞中。专性细胞内病原体的侵袭素是预防或治愈感染的有吸引力的靶标，因为阻断内化步骤会阻止这些生物的存活。吞噬嗜血曲霉侵袭素的补体定义不完全。在这里，我们报告了一种新型的嗜A.噬菌体入侵蛋白AipA的意义。吞噬嗜血曲霉在小鼠感染的。传播传播期间诱导了aipA表达。当细菌在感染HL-60细胞期间从其非感染性网状细胞形态转变为其感染性密集型形态时，该细菌上调aipA转录。 AipA定位于细菌表面，并在体内感染期间表达。在预计将被表面暴露的AipA区中，仅残基1至87（AipA_（1-87））被发现对于宿主细胞的入侵至关重要。重组AipA_（1-87）蛋白结合并竞争性抑制哺乳动物细胞的嗜A.phagocytophilum感染。特异性针对AipA_（1-87）而非其他AipA区域的抗血清可拮抗感染。使用肽特异性抗血清的其他封闭实验将AipA入侵域的范围缩小到9至21位残基。靶向AipA_（1-87）的抗血清组合以及其他两个吞噬嗜酸曲霉菌侵袭素OmpA和Asp14几乎消除了宿主细胞的感染。这项研究确定了AipA是一种对感染至关重要的吞噬曲霉表面蛋白，划定了其入侵域，并建立了针对多种侵袭素以防止粒细胞性浆膜炎的基本原理。

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