Resveratrol attenuates CXCL11 expression induced by proinflammatory cytokines in retinal pigment epithelial cells

- IFN-γ, IL-1β and TNF-α highly increased the production of CXCL11 by RPE cells.
- Resveratrol suppressed the proinflammatory cytokines-induced CXCL11 production.
- Resveratrol also blocked nuclear factor-κB activation by proinflammatory cytokines.
- Resveratrol may attenuate RPE inflammatory response implicated in AMD.

Dysfunction of the retinal pigment epithelium (RPE) resulting from chronic inflammation is implicated in the pathogenesis of age-related macular degeneration (AMD). RPE cells adjacent to drusen deposits in the AMD eye are known to contain CXCL11, a chemokine involved in inflammatory cell recruitment. We investigated the CXCL11 production by the human RPE (ARPE-19) cells under inflammatory conditions and tested its response to resveratrol, a naturally occurring anti-inflammatory antioxidant. A proinflammatory cytokine mixture consisting of IFN-γ, IL-1β and TNF-α highly increased CXCL11 mRNA expression and CXCL11 protein secretion by ARPE-19 cells. Resveratrol substantially inhibited the proinflammatory cytokines-induced CXCL11 production while partially blocking nuclear factor-κB activation. This inhibitory action of resveratrol was also observed for the cytokines-induced expression of chemokines CXCL9, CCL2 and CCL5. Our results indicate that resveratrol could potentially attenuate RPE inflammatory response implicated in the pathogenesis of AMD.