| First Author | Wang Y | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 2 | Pages | e57085 |
| PubMed ID | 23437317 | Mgi Jnum | J:197190 |
| Mgi Id | MGI:5491099 | Doi | 10.1371/journal.pone.0057085 |
| Citation | Wang Y, et al. (2013) Role of IRAK-M in alcohol induced liver injury. PLoS One 8(2):e57085 |
| abstractText | Increasing evidence suggests that innate immunity plays an important role in alcohol-induced liver injury and most studies have focused on positive regulation of innate immunity. The main objective of this study was to investigate the negative regulator of innate immunity, IL-1/Toll-like receptor (TLR) signaling pathways and interleukin receptor-associated kinase-M (IRAK-M) in alcoholic liver injury. We established an alcohol-induced liver injury model using wild type and IRAK-M deficient B6 mice and investigated the possible mechanisms. We found that in the absence of IRAK-M, liver damage by alcohol was worse with higher alanine transaminase (ALT), more immune cell infiltration and increased numbers of IFNgamma producing cells. We also found enhanced phagocytic activity in CD68(+) cells. Moreover, our results revealed altered gut bacteria after alcohol consumption and this was more striking in the absence of IRAK-M. Our study provides evidence that IRAK-M plays an important role in alcohol-induced liver injury and IRAK-M negatively regulates the innate and possibly the adaptive immune response in the liver reacting to acute insult by alcohol. In the absence of IRAK-M, the hosts developed worse liver injury, enhanced gut permeability and altered gut microbiota. |
