MicroRNAs (miRNAs) are essential post-transcriptional regulators of gene expression and have emerged as key modulators of host–pathogen interactions during bacterial infection. In this narrative review, we synthesize recent experimental and mechanistic evidence on how infection-responsive miRNAs shape innate and adaptive immunity, focusing on four representative pathogens: Salmonella, Listeria monocytogenes, Mycobacterium tuberculosis, and Helicobacter pylori. We highlight major miRNA-regulated signaling modules, including TLR/NF-κB, JAK–STAT, autophagy, immunometabolic reprogramming, and extracellular vesicle mediated intercellular communication, and summarize experimentally validated miRNA–target interactions that calibrate immune activation thresholds and inflammatory outcomes. Accumulating evidence indicates that miRNAs not only fine-tune host defense programs by controlling immune-related gene expression and immune cell activation, but can also be exploited by bacterial pathogens to suppress antimicrobial signaling and promote intracellular survival or persistent colonization. Collectively, these findings position miRNAs as a critical regulatory layer linking immune signaling networks to infection outcomes and underscore their translational potential as biomarkers and host directed therapeutic targets, while remaining grounded in current experimental evidence.
Li et al. (Tue,) studied this question.