| First Author | Shinjo T | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 477 |
| Issue | 2 | Pages | 241-6 |
| PubMed ID | 27311858 | Mgi Jnum | J:236491 |
| Mgi Id | MGI:5806202 | Doi | 10.1016/j.bbrc.2016.06.049 |
| Citation | Shinjo T, et al. (2016) IL-17A synergistically enhances TNFalpha-induced IL-6 and CCL20 production in 3T3-L1 adipocytes. Biochem Biophys Res Commun 477(2):241-6 |
| abstractText | Interleukin-17A (IL-17A) is known to induce inflammatory responses and to be involved in the pathogenesis of not only autoimmune diseases, but also several metabolic and infectious diseases. In this study, IL-17A is shown to induce IL-6 expression in 3T3-L1 mature adipocytes. Interestingly, we found that IL-17A synergistically amplified TNFalpha-induced secretion of IL-6 and upregulation of IL-17RA expression in 3T3-L1 adipocytes. Its synergistic effects on IL-6 production were inhibited by pre-treatment with inhibitors of IkappaBalpha and JNK. Furthermore, IL-17A cooperatively enhanced LPS-mediated IL-6 production in 3T3-L1 adipocytes co-cultured with RAW264.7 macrophages. In addition, IL-17A also enhanced CCL20 production in 3T3-L1 adipocytes stimulated with TNFalpha or co-cultured with LPS-stimulated RAW macrophages. In high-fat diet-fed mouse epididymal adipose tissues, IL-17RA and RORgammat mRNA levels were significantly increased and the serum level of CCL20 was also upregulated. Taken together, these data show that, in adipose tissues, IL-17A contributes to exacerbating insulin resistance-enhancing IL-6 production and promotes the infiltration of Th17 cells in cooperation with TNFalpha; these findings represent a novel hypothesis for the association between IL-17A-producing cells and type 2 diabetes. |
