# MicroRNAs as Orchestrators of Immune Responses to Bacterial Infection

## TL;DR

This paper reviews how microRNAs regulate immune responses during bacterial infections and their role in shaping host-pathogen interactions.

## Contribution

The paper synthesizes recent evidence on miRNA-regulated immune signaling during infections with four specific bacterial pathogens.

## Key findings

- miRNAs modulate innate and adaptive immunity through pathways like TLR/NF-κB and JAK–STAT.
- Bacterial pathogens can exploit miRNAs to suppress immune responses and promote survival.
- miRNAs are potential biomarkers and therapeutic targets for bacterial infections.

## Abstract

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.