Different Retinal Expression Patterns of IL-1α, IL-1β, and Their Receptors in a Rat Model of Type 1 STZ-Induced Diabetes

Diabetic retinopathy (DR), a common complication of diabetes, remains a major cause of blindness among population. Considerable amounts of evidences suggest the involvement of inflammatory process in this pathology. Increased levels of proinflammatory cytokines, including interleukin-1 beta (IL-1 beta), were found in the vitreous of diabetic patients and in the retina of diabetic rats. However, in this context, no attention has been given to the other main IL-1 family members: IL-1 alpha, two transmembrane receptors IL-1RI and IL-1RII and the natural antagonist receptor IL-1Ra. Despite that they actively participate in the IL-1-mediated inflammation process, their implication in DR has not been described. Thus, we investigated by Western blot and confocal laser scanning microscopy analysis the effect of hyperglycemia on expression of IL-1 family members in retinal layers, using an in vivo model of type 1 diabetes. It was induced in adult rats by intraperitoneal injection of streptozotocin (STZ). Exposure to hyperglycemia induces a significant increase in the protein expression of IL-1 beta, IL-1RI, IL-RII and IL-1Ra but not of IL-1 alpha. Moreover, high glucose alters their distribution pattern in the rat's retinal layers. Among these latter, the most compromised are the photoreceptor, the inner plexiform and ganglion cell layers. These findings support previous data demonstrating the involvement of inflammation in DR and suggest new pharmacological approaches for the treatment of this pathology.