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首页> 外文期刊>Infection and immunity >Contribution of Candida albicans Cell Wall Components to Recognition by and Escape from Murine Macrophages
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Contribution of Candida albicans Cell Wall Components to Recognition by and Escape from Murine Macrophages

机译：白色念珠菌细胞壁成分对小鼠巨噬细胞识别和逃逸的贡献

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The pathogenicity of the opportunistic human fungal pathogen Candida albicans depends on its ability to escape destruction by the host immune system. Using mutant strains that are defective in cell surface glycosylation, cell wall protein synthesis, and yeast-hypha morphogenesis, we have investigated three important aspects of C. albicans innate immune interactions: phagocytosis by primary macrophages and macrophage cell lines, hyphal formation within macrophage phagosomes, and the ability to escape from and kill macrophages. We show that cell wall glycosylation is critically important for the recognition and ingestion of C. albicans by macrophages. Phagocytosis was significantly reduced for mutants deficient in phosphomannan biosynthesis (mmn4Δ, pmr1Δ, and mnt3 mnt5Δ), whereas O- and N-linked mannan defects (mnt1Δ mnt2Δ and mns1Δ) were associated with increased ingestion, compared to the parent wild-type strains and genetically complemented controls. In contrast, macrophage uptake of mutants deficient in cell wall proteins such as adhesins (ece1Δ, hwp1Δ, and als3Δ) and yeast-locked mutants (clb2Δ, hgc1Δ, cph1Δ, efg1Δ, and efg1Δ cph1Δ), was similar to that observed for wild-type C. albicans. Killing of macrophages was abrogated in hypha-deficient strains, significantly reduced in all glycosylation mutants, and comparable to wild type in cell wall protein mutants. The diminished ability of glycosylation mutants to kill macrophages was not a consequence of impaired hyphal formation within macrophage phagosomes. Therefore, cell wall composition and the ability to undergo yeast-hypha morphogenesis are critical determinants of the macrophage's ability to ingest and process C. albicans.
机译：机会性人类真菌病原体白色念珠菌的致病性取决于其逃脱宿主免疫系统破坏的能力。使用在细胞表面糖基化，细胞壁蛋白合成和酵母菌丝形态发生方面有缺陷的突变株，我们研究了C的三个重要方面。白色念珠菌固有免疫相互作用：原代巨噬细胞和巨噬细胞细胞系的吞噬作用，巨噬细胞吞噬体中的菌丝形成以及逃避和杀死巨噬细胞的能力。我们表明，细胞壁糖基化对于识别和摄取C至关重要。巨噬细胞的白色念珠菌。磷酸甘露聚糖生物合成不足的突变体（ mmn4 Δ， pmr1 Δ和 mnt3 mnt5 Δ）的吞噬作用显着降低，而O-和N-与亲本野生型菌株相比，连锁的甘露聚糖缺陷（ mnt1 Δ mnt2 Δ和 mns1 Δ）与摄食增加有关，并且具有遗传互补性控制。相反，缺乏细胞壁蛋白（例如粘附素（ ece1 Δ， hwp1 Δ和 als3 Δ））和酵母菌的突变体的巨噬细胞摄取锁定的突变体（ clb2 Δ， hgc1 Δ， cph1 Δ， efg1 Δ和 efg1 Δ cph1 Δ），与野生型 C观察到的相似。白色的。在噬菌体缺陷型菌株中废除了巨噬细胞的杀伤，在所有糖基化突变体中均明显减少，与细胞壁蛋白突变体中的野生型相当。糖基化突变体杀死巨噬细胞的能力降低不是巨噬细胞吞噬体中菌丝形成受损的结果。因此，细胞壁组成和经历酵母菌丝形态发生的能力是巨噬细胞摄取和加工C的能力的关键决定因素。白色的。

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