Oncotarget

Research Papers: Immunology:

SNX10 promotes phagosome maturation in macrophages and protects mice against Listeria monocytogenes infection

Jun Lou, Xiawei Li, Wei Huang, Jingjing Liang, Mingzhu Zheng, Ting Xu, Jun Lyu, Dan Li, Qin Xu, Xuexiao Jin, Guotong Fu, Di Wang and Linrong Lu _

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Oncotarget. 2017; 8:53935-53947. https://doi.org/10.18632/oncotarget.19644

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Abstract

Jun Lou1,2,*, Xiawei Li1,2,*, Wei Huang1,2, Jingjing Liang1,2, Mingzhu Zheng1,2, Ting Xu1,2, Jun Lyu1,2, Dan Li1,2, Qin Xu1,2, Xuexiao Jin1,2, Guotong Fu1,2, Di Wang1,2 and Linrong Lu1,2

1 Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, China

2 Program in Molecular and Cellular Biology, Zhejiang University School of Medicine, Hangzhou, China

* These authors have equally contributed to this work

Correspondence to:

Linrong Lu, email:

Keywords: SNX10, macrophage, Listeria monocytogenes, phagosome, innate immunity, Immunology and Microbiology Section, Immune response, Immunity

Received: May 16, 2017 Accepted: July 13, 2017 Published: July 27, 2017

Abstract

Listeria monocytogenes (L. monocytogenes),which is a facultative intracellular bacterial pathogen that causes listeriosis, is widely used to study the mammalian immune response to infection. After phagocytosis by professional phagocytes, L. monocytogenes is initially contained within phagosomes, which mature into phagolysosomes, where the bacteria are degraded. Although phagocytosis and subsequent phagosome maturation is essential for the clearance of infectious microbial pathogens, the underlying regulatory mechanisms are still unclear. SNX10 (Sorting nexin 10) has the simplest structure of the SNX family and has been reported to regulate endosomal morphology, which might be crucial for macrophage function, including phagocytosis and digestion of pathogens, inflammatory response, and antigen presentation. Our results showed that SNX10 expression was upregulated following L. monocytogenes infection in macrophages. It was also revealed that SNX10 promoted phagosome maturation by recruiting the Mon1-Ccz1 complex to endosomes and phagosomes. As a result, SNX10 deficiency decreased the bacterial killing ability of macrophages, and SNX10-deficient mice showed increased susceptibility to L. monocytogenes infection in vivo. Thus, this study revealed an essential role of SNX10 in controlling bacterial infection.


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