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Oncotarget. 2017 Jul 27;8(33):53935-53947. doi: 10.18632/oncotarget.19644. eCollection 2017 Aug 15.

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

Lou J#1,2, Li X#1,2, Huang W1,2, Liang J1,2, Zheng M1,2, Xu T1,2, Lyu J1,2, Li D1,2, Xu Q1,2, Jin X1,2, Fu G1,2, Wang D1,2, Lu L1,2.

Author information

Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Program in Molecular and Cellular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Contributed equally


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.


Immune response; Immunity; Immunology and Microbiology Section; Listeria monocytogenes; SNX10; innate immunity; macrophage; phagosome

Conflict of interest statement

CONFLICTS OF INTEREST All authors reported no conflict of interest.

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