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鸟分枝杆菌感染的巨噬细胞中的胆固醇消耗克服了吞噬体成熟的障碍,并导致活的分枝杆菌在吞噬溶酶体衍生的自噬泡中可逆性隔离。

Cholesterol depletion in Mycobacterium avium-infected macrophages overcomes the block in phagosome maturation and leads to the reversible sequestration of viable mycobacteria in phagolysosome-derived autophagic vacuoles.

作者信息

de Chastellier Chantal, Thilo Lutz

机构信息

Centre d'Immunologie de Marseille-Luminy, INSERM-CNRS-Université de la Méditerranée, Marseille, France.

出版信息

Cell Microbiol. 2006 Feb;8(2):242-56. doi: 10.1111/j.1462-5822.2005.00617.x.

Abstract

Phagocytic entry of mycobacteria into macrophages requires the presence of cholesterol in the plasma membrane. This suggests that pathogenic mycobacteria may require cholesterol for their subsequent intra-cellular survival in non-maturing phagosomes. Here we report on the effect of cholesterol depletion on pre-existing phagosomes in mouse bone marrow-derived macrophages infected with Mycobacterium avium. Cholesterol depletion with methyl-beta-cyclodextrin resulted in a loosening of the close apposition between the phagosome membrane and the mycobacterial surface, followed by fusion with lysosomes. The resulting phagolysosomes then autonomously executed autophagy, which did not involve the endoplasmic reticulum. After 5 h of depletion, intact mycobacteria had accumulated in large auto-phagolysosomes. Autophagy was specific for phagolysosomes that contained mycobacteria, as it did not involve latex bead-containing phagosomes in infected cells. Upon replenishment of cholesterol, mycobacteria became increasingly aligned to the lysosomal membrane, from where they were individually sequestered in phagosomes with an all-around closely apposed phagosome membrane and which no longer fused with lysosomes. These observations indicate that, cholesterol depletion (i) resulted in phagosome maturation and fusion with lysosomes and (ii) caused mycobacterium-containing phagolysosomes to autonomously undergo autophagy. Furthermore, (iii) mycobacteria were not killed in auto-phagolysosomes, and (iv) cholesterol replenishment enabled mycobacterium to rescue itself from autophagic phagolysosomes to again reside individually in phagosomes which no longer fused with lysosomes.

摘要

分枝杆菌通过吞噬作用进入巨噬细胞需要质膜中存在胆固醇。这表明致病性分枝杆菌在未成熟吞噬体中的细胞内存活可能需要胆固醇。在此,我们报告了胆固醇耗竭对感染鸟分枝杆菌的小鼠骨髓来源巨噬细胞中预先存在的吞噬体的影响。用甲基-β-环糊精耗竭胆固醇导致吞噬体膜与分枝杆菌表面之间紧密贴附关系松弛,随后与溶酶体融合。产生的吞噬溶酶体随后自主执行自噬,这一过程不涉及内质网。耗竭5小时后,完整的分枝杆菌积聚在大型自噬吞噬溶酶体中。自噬对含有分枝杆菌的吞噬溶酶体具有特异性,因为它不涉及感染细胞中含有乳胶珠的吞噬体。补充胆固醇后,分枝杆菌越来越多地与溶酶体膜对齐,从那里它们被单独隔离在吞噬体中,吞噬体膜四周紧密贴附,且不再与溶酶体融合。这些观察结果表明,胆固醇耗竭(i)导致吞噬体成熟并与溶酶体融合,(ii)使含有分枝杆菌的吞噬溶酶体自主发生自噬。此外,(iii)分枝杆菌在自噬吞噬溶酶体中未被杀死,(iv)补充胆固醇使分枝杆菌能够从自噬吞噬溶酶体中解救自身,再次单独存在于不再与溶酶体融合的吞噬体中。

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