Erschienen in:
01.04.2012
IL-33 Is Induced by Amyloid-β Stimulation and Regulates Inflammatory Cytokine Production in Retinal Pigment Epithelium Cells
verfasst von:
Xiao-Cui Liu, Xiao-Fei Liu, Cong-Xiang Jian, Chen-Jun Li, Shou-Zhi He
Erschienen in:
Inflammation
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Ausgabe 2/2012
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Abstract
Age-related macular degeneration (AMD) is the predominant cause of irreversible blindness in the elderly population. Despite intensive basic and clinical research, its pathogenesis remains unclear. However, evidence suggests that immunological and inflammatory factors contribute to the pathogenesis of AMD. A newly identified cytokine, IL-33, appears to be an important pro-inflammatory cytokine promoting tissue inflammation. In this study, IL-33 was increased through amyloid-beta1–40 (Aβ1–40) stimulation and regulated inflammatory cytokines including IL-6, IL-8, IL-1β, and TNF-α secretion using different signaling pathways in retinal pigment epithelium (RPE) cells. Furthermore, ST2L, the important component of the IL-33 receptor, was significantly increased following recombinant human IL-33 stimulation in RPE cells. These findings suggest that IL-33-mediated inflammatory responses in RPE cells are involved in the pathogenesis of AMD. Greater understanding of the inflammatory effect of IL-33 and its role in RPE cells should aid the development of future clinical therapeutics and enable novel pharmacological approaches towards the prevention of AMD.