MA RNA Methylation Mediates NOD1/NF-kB Signaling Activation in the Liver of Piglets Challenged with Lipopolysaccharide.

N-methyladenosine (mA) is the most abundant internal modification that widely participates in various immune and inflammatory responses; however, its regulatory mechanisms in the inflammation of liver induced by lipopolysaccharide in piglets remain largely unknown. In the present study, piglets were intraperitoneally injected with 80 μg/kg LPS or an equal dose of sterile saline. Results indicated that LPS administration increased activities of serum alanine aminotransferase (ALT), induced M1 macrophage polarization and promoted secretion of inflammatory cytokines, and finally led to hepatic lesions in piglets.

The regulatory role of N -methyladenosine modification in the interaction between host and microbes.

N -methyladenosine (m A) is the most prevalent posttranscriptional modification in eukaryotic mRNAs. Dynamic and reversible m A modification regulates gene expression to control cellular processes and diverse biological functions. Growing evidence indicated that m A modification is involved in the homeostasis of host and microbes (mostly viruses and bacteria).

Resveratrol Attenuates Aflatoxin B-Induced ROS Formation and Increase of mA RNA Methylation.

Aflatoxin B (AFB) is one of the most dangerous mycotoxins in both humans and animals. Regulation of resveratrol is essential for the inhibition of AFB-induced oxidative stress and liver injury. Whether N-methyladenosine (mA) mRNA methylation participates in the crosstalk between resveratrol and AFB is unclear.