Human bFGF adenoviral particles

IL-17 is a pro-inflammatory cytokine that has been implicated in a variety of autoimmune diseases. FGF2 synergizes with IL-17 to protect the intestinal epithelium during dextran sodium sulfate (DSS)-induced colitis. Here, researchers investigated the pathogenic role of FGF2-IL-17 synergy in the pathogenesis of autoimmune arthritis. Combination treatment with FGF2 and IL-17 synergistically induced ERK activation and cytokine and chemokine production in human synovial intimal resident fibroblast-like synoviocytes (FLS). Furthermore, ectopic expression of FGF2 in mouse joints enhanced IL-17-induced inflammatory cytokine and chemokine production in tissues. In a collagen-induced arthritis (CIA) model, while ectopic expression of FGF2 in vivo exacerbated tissue inflammation and disease symptoms in wild-type controls, this effect was greatly attenuated in Il17a^−/− mice. Together, these studies suggest that FGF2 cooperates with IL-17 to induce inflammatory responses, thereby contributing to the pathogenesis of autoimmune arthritis.

Here, to determine whether FGF2 works synergistically with IL-17 in vivo, the researchers injected adenovirus expressing FGF2 and/or IL-17 into the joints of healthy mice. Consistent with the in vitro data, FGF2 worked synergistically with IL-17 to induce pro-inflammatory genes in the joint tissues of mice (Figure 1A). Histological analysis showed that simultaneous expression of FGF2 and IL-17 resulted in more severe tissue swelling and immune cell infiltration than that induced by either cytokine alone (Figure 1B). These results suggest that FGF2 and IL-17 may synergistically promote joint inflammation.

Figure 1. FGF2 synergizes with IL-17 to promote inflammatory pathogenesis. (Shao X, et al., 2017)