Proteomics reveals the potential mechanism of Mrps35 controlling Listeria intracellular proliferation in macrophages.

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

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 infected macrophages. Our results indicated that knockdown Mrps35 increased the load of Listeria in macrophages. This result supported that Mrps35 played the crucial roles in Listeria infection. Moreover, we performed the comprehensive proteomics to analyze the differentially expressed protein of wild type and Mrps35 Knockdown Raw264.7 cells by Listeria infection over 6h. Based on the results of mass spectrometry, we presented a wide variety of hypotheses about the mechanism of Mrps35 controlling the Listeria 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 Listeria infection. This study provided new insights into understanding that Listeria infection changed the basic synthesis or metabolism-related proteins of host cells. This article is protected by copyright. All rights reserved.