| First Author | Wernstedt Asterholm I | Year | 2016 |
| Journal | Am J Pathol | Volume | 186 |
| Issue | 9 | Pages | 2404-16 |
| PubMed ID | 27397737 | Mgi Jnum | J:235058 |
| Mgi Id | MGI:5792738 | Doi | 10.1016/j.ajpath.2016.04.017 |
| Citation | Wernstedt Asterholm I, et al. (2016) Pathological Type-2 Immune Response, Enhanced Tumor Growth, and Glucose Intolerance in Retnlbeta (RELMbeta) Null Mice: A Model of Intestinal Immune System Dysfunction in Disease Susceptibility. Am J Pathol 186(9):2404-16 |
| abstractText | Resistin, and its closely related homologs, the resistin-like molecules (RELMs) have been implicated in metabolic dysregulation, inflammation, and cancer. Specifically, RELMbeta, expressed predominantly in the goblet cells in the colon, is released both apically and basolaterally, and is hence found in both the intestinal lumen in the mucosal layer as well as in the circulation. RELMbeta has been linked to both the pathogenesis of colon cancer and type 2 diabetes. RELMbeta plays a complex role in immune system regulation, and the impact of loss of function of RELMbeta on colon cancer and metabolic regulation has not been fully elucidated. We therefore tested whether Retnlbeta (mouse ortholog of human RETNLbeta) null mice have an enhanced or reduced susceptibility for colon cancer as well as metabolic dysfunction. We found that the lack of RELMbeta leads to increased colonic expression of T helper cell type-2 cytokines and IL-17, associated with a reduced ability to maintain intestinal homeostasis. This defect leads to an enhanced susceptibility to the development of inflammation, colorectal cancer, and glucose intolerance. In conclusion, the phenotype of the Retnlbeta null mice unravels new aspects of inflammation-mediated diseases and strengthens the notion that a proper intestinal barrier function is essential to sustain a healthy phenotype. |
