4.4 Article

MicroRNAs Contribute to Host Response to Coxiella burnetii

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INFECTION AND IMMUNITY
卷 91, 期 1, 页码 -

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AMER SOC MICROBIOLOGY
DOI: 10.1128/iai.00199-22

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Coxiella burnetii; miRNA; macrophage; apoptosis; autophagy; infection

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MicroRNAs (miRNAs) play a critical role in gene regulation and are involved in modulating various physiological processes, including the host response to intracellular infections. This study investigates the miRNA expression in macrophages infected with C. burnetii and identifies several differentially expressed miRNAs. Specifically, miR-143-3p, whose expression is downregulated during C. burnetii infection, promotes apoptosis and inhibits autophagy, thereby benefiting the pathogen.
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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