Simple Summary: miR-129a-3p plays an important role in the inflammatory response induced by G. parasuis infection. The TLR4/NF-κB signaling
Simple Summary: miR-129a-3p plays an important role in the inflammatory response induced by G. parasuis infection. The TLR4/NF-κB signaling pathway is an important inflammatory signaling pathway. The results of this study showed that miR-129a-3p targeted the TLR4/NF-κB signaling pathway to regulate the inflammatory injury caused by G. parasuis-infected porcine alveolar macrophage cells, providing new insights into the role of miRNA in the pathogenic mechanism G. parasuis. Glaesserella parasuis (G. parasuis) is the primary pathogen responsible for Glässer's disease and poses a significant threat to the global pig industry. MicroRNAs are a class of short, endogenous, single-stranded noncoding RNAs that play crucial roles in inflammation, apoptosis, proliferation, differentiation, and invasion in various organisms. This study analyzed the characteristics of porcine alveolar macrophage (PAM) cells infected with G. parasuis through the knockdown and overexpression of ssc-miR-129a-3p. We constructed a cellular model with ssc-miR-129a-3p knockdown invaded by G. parasuis strain XX0306, screening 160 differentially expressed genes via high-throughput sequencing. GO enrichment analysis revealed that 376 GO entries were enriched. KEGG enrichment analysis found that mRNA target genes were enriched in 17 cell signaling pathways, including G protein-coupled components, PPAR, and other signaling pathways that can mediate inflammatory pathways. By examining the expression of relevant inflammatory factors and signaling pathways, we elucidated the molecular mechanisms through which ssc-miR-129a-3p targets the TLR4/NF-κB signaling pathway to regulate inflammatory injury. This study establishes a foundation for further research into the role of miRNA in the pathogenesis of Glässer disease and is highly significant for the prevention and control of bacterial diseases within the pig industry. [ABSTRACT FROM AUTHOR]
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