miR-215 Modulates Ubiquitination to Impair Inflammasome Activation and Autophagy During Salmonella Typhimurium Infection in Porcine Intestinal Cells

Simple summary: In this study, we investigated the role of microRNA-215 (miR-215) during Salmonella Typhimurium (S. Typhimurium) infection using a combination of in vivo porcine models and in vitro epithelial cell lines. Several dysregulated microRNAs (miRNAs) were identified in the infected porcine ileum, with miR-215 showing significant downregulation. Gain-of-function experiments in porcine (IPEC-J2) and human (HT29) intestinal epithelial cells revealed that miR-215 overexpression inhibits ubiquitination, subsequently downregulating key host immune response pathways such as autophagy and inflammasome activation. Our findings demonstrate that miR-215, downregulated during Salmonella Typhimurium infection in porcine ileum, plays a crucial role in regulating the host immune response by targeting proteins involved in ubiquitination, thereby influencing inflammasome activation and autophagy.