Phagocytosis of Candida albicans Inhibits Autophagic Flux in Macrophages.
Phagocytosis of Candida albicans Inhibits Autophagic Flux in Macrophages.
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白色念珠菌的吞噬作用抑制巨噬细胞的自噬流
DOI：
10.1155/2018/4938649
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发表时间：
2018
影响因子：
--
通讯作者：
Li M
中科院分区：
文献类型：
--
作者：
Duan Z;Chen Q;Du L;Tong J;Xu S;Zeng R;Ma Y;Chen X;Li M
自噬机制在防御微生物如白色念珠菌中起作用。脂化LC 3是自噬的标志蛋白，参与C.通过形成单膜吞噬体来吞噬白色念珠菌;该过程称为LC 3相关吞噬作用（LC 3-associated phagocytosis，简称LPS）。然而，C.白念珠菌对自噬通量的影响尚不清楚。在本研究中，我们发现C.白念珠菌抑制巨噬细胞中LC 3的更新。C.在巨噬细胞中，我们观察到较少的吖啶橙阳性空泡和RFP-GFP-LC 3斑点，而没有与吞噬的C.白色念珠菌。但C.白色念珠菌导致LC 3募集，但p62和ATG 9A不与LC 3或C.白色念珠菌。这些效应是由于MTOR非依赖性途径。然而，我们发现C.白念珠菌模式相关分子模式β-葡聚糖增加LC 3周转。此外，C.白色念珠菌引起BrdU掺入减少。阻断自噬流加重了这种效应。我们的研究结果表明，C。白色念珠菌减少自噬通量，但在巨噬细胞中以MTOR非依赖性方式诱导自噬。招募人员占领LC 3吞没了C。白念珠菌可能参与了自噬流的抑制。我们的研究强调了典型的自噬和防御C.白色念珠菌攻毒。
Autophagy machinery has roles in the defense against microorganisms such as Candida albicans. Lipidated LC3, the marker protein of autophagy, participates in the elimination of C. albicans by forming a single-membrane phagosome; this process is called LC3-associated phagocytosis (LAP). However, the influence of C. albicans on autophagic flux is not clear. In this study, we found that C. albicans inhibited LC3 turnover in macrophages. After the phagocytosis of C. albicans in macrophages, we observed fewer acridine orange-positive vacuoles and RFP-GFP-LC3 puncta without colocalization with phagocytized C. albicans. However, phagocytosis of C. albicans led to LC3 recruitment, but p62 and ATG9A did not colocalize with LC3 or C. albicans. These effects are due to an MTOR-independent pathway. Nevertheless, we found that the C. albicans pattern-associated molecular pattern β-glucan increased LC3 turnover. In addition, phagocytosis of C. albicans caused a decrease in BrdU incorporation. Blocking autophagic flux aggravated this effect. Our findings suggest that phagocytosis of C. albicans decreases autophagic flux but induces LAP in an MTOR-independent manner in macrophages. Occupation of LC3 by recruiting engulfed C. albicans might contribute to the inhibition of autophagic flux. Our study highlights the coordinated machinery between canonical autophagy and LAP that defends against C. albicans challenge.
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影响因子：
2.9
作者：
Rosentul DC;Plantinga TS;Farcas M;Oosting M;Hamza OJ;Scott WK;Alexander BD;Yang JC;Laird GM;Joosten LA;van der Meer JW;Perfect JR;Kullberg BJ;van der Ven AJ;Johnson MD;Netea MG
通讯作者：
Netea MG
影响因子：
7.3
作者：
Lamprinaki D;Beasy G;Zhekova A;Wittmann A;James S;Dicks J;Iwakura Y;Saijo S;Wang X;Chow CW;Roberts I;Korcsmaros T;Mayer U;Wileman T;Kawasaki N
通讯作者：
Kawasaki N
影响因子：
21.3
作者：
通讯作者：
--
p62/SQSTM1形成自噬降解的蛋白质聚集体，并对亨廷顿蛋白诱导的细胞死亡具有保护作用。
影响因子：
7.8
作者：
Bjorkoy, Geir;Lamark, Trond;Brech, Andreas;Outzen, Heidi;Perander, Maria;Overvatn, Aud;Stenmark, Harald;Johansen, Terje
通讯作者：
Johansen, Terje
影响因子：
16.6
作者：
Kanayama, Masashi;Inoue, Makoto;Danzaki, Keiko;Hammer, Gianna;He, You-Wen;Shinohara, Mari L.
通讯作者：
Shinohara, Mari L.