| First Author | Zhang J | Year | 2019 |
| Journal | Mol Immunol | Volume | 107 |
| Pages | 132-141 | PubMed ID | 30738250 |
| Mgi Jnum | J:295288 | Mgi Id | MGI:6453792 |
| Doi | 10.1016/j.molimm.2019.01.018 | Citation | Zhang J, et al. (2019) MLKL deficiency inhibits DSS-induced colitis independent of intestinal microbiota. Mol Immunol 107:132-141 |
| abstractText | The maintenance of intestinal tissue homeostasis is vital for the resistance against inflammatory bowel diseases (IBDs). Necroptosis is identified as an alternative mode of regulated cell death, which plays a pivotal role in tissue homeostasis. Thus, the roles of RIP3-mediated necroptosis in intestinal inflammation have been extensively studied. However, the biological implications of the mixed lineage kinase-like protein (MLKL), a molecule downstream of RIP3 in gut remain unclear. In this study, the role of MLKL in DSS-induced colitis was examined, and the contribution of gut microbiota was also determined. Compared with non-littermate WT mice, the survival rate, clinical score, intestinal damage and intestinal mucosal barrier integrity of non-littermate MLKL-deficient mice are significantly improved. MLKL deficiency prevents inflammatory cytokines production and MAPK signaling activation. Hence, MLKL deficiency inhibits DSS-induced colitis. Moreover, we proved that DSS susceptibility difference between two genotypes is not driven by intestinal microbiota based on the co-housing of two non-littermate genotypes and qPCR detection of fecal dominant bacterial taxa. |
