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Proteomics reveals the potential mechanism of Mrps35 controlling Listeria monocytogenes intracellular proliferation in macrophages
Author(s) -
Yuan Jiangbei,
Li Zhangfu,
Li Fang,
Lin Zewei,
Yao Siyu,
Zhou Hang,
Liu Wenhu,
Yu Haili,
Liu Yang,
Liu Fang,
Li Fei,
Ran Haiying,
Zhang Junying,
Huang Yi,
Fu Qihuan,
Wang Liting,
Liu Jikui
Publication year - 2021
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.202000262
Subject(s) - listeria monocytogenes , ribosomal protein , proteomics , gene knockdown , intracellular , biology , microbiology and biotechnology , phagocytosis , bacteria , intracellular parasite , rna , biochemistry , apoptosis , ribosome , genetics , gene
Macrophages are sentinels in the organism which can resist and destroy various bacteria through direct phagocytosis. Here, we reported that expression level of mitochondrial ribosomal protein S35 (Mrps35) continued to decrease over infection time after Listeria monocytogenes ( L. monocytogenes ) infected macrophages. Our results indicated that knockdown Mrps35 increased the load of L. monocytogenes in macrophages. This result supported that Mrps35 played the crucial roles in L. monocytogenes infection. Moreover, we performed the comprehensive proteomics to analyze the differentially expressed protein of wild type and Mrps35 Knockdown Raw264.7 cells by L. monocytogenes infection over 6 h. Based on the results of mass spectrometry, we presented a wide variety of hypotheses about the mechanism of Mrps35 controlling the L. monocytogenes intracellular proliferation. Among them, experiments confirmed that Mrps35 and 60S ribosomal protein L22‐like 1 (Rpl22l1) were a functional correlation or potentially a compensatory mechanism during L. monocytogenes infection. This study provided new insights into understanding that L. monocytogenes infection changed the basic synthesis or metabolism‐related proteins of host cells.