MicroRNAs at the Host–Bacteria Interface: Host Defense or Bacterial Offense

• Published in: Trends in microbiology (Regular ed.) Vol. 27; no. 3; pp. 206 - 218
• Main Authors: Aguilar, Carmen, Mano, Miguel, Eulalio, Ana
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.03.2019; Elsevier Science Ltd
• Subjects: Bacteria; bacterial pathogen; Cell interactions; cell-to-cell communication; Crosstalk; Gene expression; host–pathogen interaction; Immune response; Immune system; Infections; Microbiota; microRNA; MicroRNAs; miRNA; Pathogens; Post-transcription; Regulators; microbiota; microRNA; cell-to-cell communication; bacterial pathogen; host–pathogen interaction
• ISSN: 0966-842X; 1878-4380
• DOI: 10.1016/j.tim.2018.10.011

MicroRNAs are a class of small noncoding RNAs that act as major post-transcriptional regulators of gene expression. They are currently recognized for their important role in the intricate interaction between host and bacterial pathogens, either as part of the host immune response to neutralize infection, or as a molecular strategy employed by bacteria to hijack host pathways for their own benefit. Here, we summarize recent advances on the function of miRNAs during infection of mammalian hosts by bacterial pathogens, highlighting key cellular pathways. In addition, we discuss emerging themes in this field, including the participation of miRNAs in host–microbiota crosstalk and cell-to-cell communication. MiRNAs have recently emerged as major players in the interactions between host and bacterial pathogens. Several host functions have been shown to be regulated by miRNAs during infection, including cell cycle, cytoskeleton organization, autophagy, cell death, and survival. MiRNAs are an integral part of the host immune response to bacterial infection. Bacterial pathogens subvert host miRNA expression for their own benefit, promoting survival, replication, and persistence. A growing number of studies indicate that gut microbiota can influence the miRNome, and vice-versa.