MicroRNAs Contribute to Host Response to Coxiella burnetii

被引:1
作者
Sachan, Madhur [1 ,2 ]
Brann, Katelynn R. [3 ]
Fullerton, Marissa S. [3 ]
Voth, Daniel E. [3 ]
Raghavan, Rahul [1 ,4 ]
机构
[1] Portland State Univ, Dept Biol, Portland, OR 97201 USA
[2] Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Cardiovasc Div, Boston, MA USA
[3] Univ Arkansas Med Sci, Dept Microbiol & Immunol, Little Rock, AR USA
[4] Univ Texas San Antonio, Dept Mol Microbiol & Immunol, San Antonio, TX 78249 USA
基金
美国国家卫生研究院;
关键词
Coxiella burnetii; miRNA; macrophage; apoptosis; autophagy; infection; CERVICAL-CANCER; ACTIVATION; APOPTOSIS; AUTOPHAGY; PATHWAY; INHIBITION; EXPRESSION; MIR-143; GROWTH; CELLS;
D O I
10.1128/iai.00199-22
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
MicroRNAs (miRNAs), a class of small noncoding RNAs, are critical to gene regulation in eukaryotes. They are involved in modulating a variety of physiological processes, including the host response to intracellular infections. MicroRNAs (miRNAs), a class of small noncoding RNAs, are critical to gene regulation in eukaryotes. They are involved in modulating a variety of physiological processes, including the host response to intracellular infections. Little is known about miRNA functions during infection by Coxiella burnetii, the causative agent of human Q fever. This bacterial pathogen establishes a large replicative vacuole within macrophages by manipulating host processes such as apoptosis and autophagy. We investigated miRNA expression in C. burnetii-infected macrophages and identified several miRNAs that were down- or upregulated during infection. We further explored the functions of miR-143-3p, an miRNA whose expression is downregulated in macrophages infected with C. burnetii, and show that increasing the abundance of this miRNA in human cells results in increased apoptosis and reduced autophagy-conditions that are unfavorable to C. burnetii intracellular growth. In sum, this study demonstrates that C. burnetii infection elicits a robust miRNA-based host response, and because miR-143-3p promotes apoptosis and inhibits autophagy, downregulation of miR-143-3p expression during C. burnetii infection likely benefits the pathogen.
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页数:13
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