Abstract
Eosinophils are proinflammatory granulocytes that are involved in the pathogenesis of various inflammatory reactions. However, their roles in psoriasis remain largely unknown. In this study, by examining the inflammatory features of the eosinophilic cell line EoL-1 and an imiquimod-induced murine model of psoriasis, we show that eosinophils provide inflammatory signals that accelerate the pathogenesis of psoriasis. EoL-1 cells constitutively expressed TLR7, which mediates acute and rapidly developing psoriatic inflammation. The activation of TLR7 on EoL-1 cells using R837 resulted in the secretion of inflammatory mediators that support the migration, activation, and survival of neutrophils. The underlying pathologic role of eosinophils in psoriatic inflammation was further substantiated by markedly decreased psoriasiform inflammation in imiquimod-treated ΔdblGATA mice, which have a systemic eosinophil deficiency. While imiquimod-treated wild-type mice showed a significant increase in the eosinophils in their skin, neutrophils remarkably outnumbered the eosinophils in the skin, lymph nodes, and spleen in wild-type mice after imiquimod application. In addition, lesional skin samples from psoriasis patients also showed up-regulated eosinophil cytotoxic granules, accompanied by marked neutrophil infiltration. Based on these collective data, we propose that eosinophils accelerate psoriatic inflammation by supporting inflammatory microenvironments to favor the activation and infiltration of neutrophils.
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