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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >CD14-Mac-1 interactions in Bacillus anthracis spore internalization by macrophages
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CD14-Mac-1 interactions in Bacillus anthracis spore internalization by macrophages

机译：巨噬细胞在炭疽芽孢杆菌孢子内在化过程中的CD14-Mac-1相互作用

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摘要

Anthrax, a potentially lethal disease of animals and humans, is caused by the Gram-positive spore-forming bacterium Bacillus anthracis. The outermost exosporium layer of B. anthracis spores contains an external hair-like nap formed by the glycoprotein BclA. Recognition of BclA by the integrin Mac-1 promotes spore uptake by professional phagocytes, resulting in the carriage of spores to sites of spore germination and bacterial growth in distant lym-phoid organs. We show that CD14 binds to rhamnose residues of BclA and acts as a coreceptor for spore binding by Mac-1. In this process, CD14 induces signals involving TLR2 and PI3k that promote inside-out activation of Mac-1, thereby enhancing spore internalization by macrophages. As observed with mice lacking Mac-1, CD14~(-/-) mice are also more resistant than wild-type mice to infection by B, anthracis spores. Additionally, after B. anthracis spore challenge of CD14~(-/-) mice, interference with the CD14-mediated signaling pathways results in increased mortality. Our results show that the binding and uptake of B. anthracis spores by phagocytic cells is a dynamic process and involves multiple receptors and signaling pathways.
机译：炭疽是革兰氏阳性孢子形成细菌炭疽芽孢杆菌（Bacillus anthracis）引起的，可能是一种致命的动物和人类疾病。炭疽芽孢杆菌孢子的最外孢子囊层含有由糖蛋白BclA形成的外部毛状小睡。整合素Mac-1对BclA的识别可促进专业吞噬细胞吸收孢子，从而将孢子运送到孢子萌发部位，并在远端的淋巴器官中生长细菌。我们显示CD14绑定到BclA的鼠李糖残基，并充当Mac-1孢子结合的共受体。在此过程中，CD14诱导涉及TLR2和PI3k的信号，这些信号促进Mac-1的内外激活，从而增强巨噬细胞对孢子的内在化。正如缺乏Mac-1的小鼠所观察到的，CD14〜（-/-）小鼠也比野生型小鼠更能抵抗炭疽芽孢杆菌的感染。此外，在炭疽芽孢杆菌对CD14〜（-/-）小鼠进行孢子攻击后，干扰CD14介导的信号通路会导致死亡率增加。我们的结果表明，吞噬细胞对炭疽芽孢杆菌的结合和吸收是一个动态过程，涉及多个受体和信号传导途径。

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