m6A RNA methylation mediates NOD1/NF-kB signaling activation in the liver of piglets challenged with lipopolysaccharide

N6-methyladenosine (m6A) is the most abundant internal modification that widely participates in various immune and inflammatory responses, however, its regulatory mechanisms in the inflam-mation of liver induced by lipopolysaccharide in piglets remain largely unknown. In the present study, MeRIP-seq showed that 1166 and 1344 transcripts contained m6A methylation in control and LPS groups, respectively. The m6A methylation sites of these transcripts mainly distributes in the 5’ un-translated region (5’UTR), the coding sequence (CDS), and the 3’ untranslated region (3’UTR). In-terestingly, these genes were mostly enriched in the NF-κB signaling pathway, and LPS treatment significantly changed the m6A modification among NOD1, RIPK2, NFKBIA, NFKBIB and TNFAIP3 mRNAs.In conclusion, LPS activated the NOD1/NF-κB pathway at post-transcriptional regulation through changing m6A RNA methylation, and then promoted the overproduction of proinflammatory cytokines, ultimately resulting in liver inflammation and damage. Twelve male piglets in the growing stages (Duroc x Large White x Landrace) were assigned randomly to two treatment groups: the control (CON) group and the Lipopolysaccharide (LPS) group.