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• W2802674887 abstract "Air pollution associated with ozone exposure represents a major inducer of respiratory disease in man. In mice, a single ozone exposure causes lung injury with disruption of the respiratory barrier and inflammation. We investigated the role of interleukin-1 (IL-1)-associated cytokines upon a single ozone exposure (1ppm for 1h) using IL-1α-, IL-1β- and IL-18- deficient mice or an anti-IL-1α neutralizing antibody underlying the rapid epithelial cell death. Here we demonstrate the release of the alarmin IL-1α after ozone exposure and that the acute respiratory barrier injury and inflammation and airway hyperreactivity are IL-1α dependent. IL-1α signaling via IL-1R1 depends on the adaptor protein MyD88. Importantly, epithelial cell signaling is critical, since deletion of MyD88 in lung type I alveolar epithelial cells reduced ozone-induced inflammation. In addition, intratracheal injection of rmIL-1α in MyD88ACID mice led to reduction of inflammation in comparison with WT mice treated with recombinant. Therefore, a major part of inflammation is mediated by IL-1α signaling in epithelial cells. In conclusion, the alarmin IL-1α released upon ozone-induced tissue damage and inflammation is mediated by MyD88 signaling in epithelial cells. Therefore, IL-1α may represent a therapeutic target to attenuate ozone-induced lung inflammation and hyperreactivity." @default.
• W2802674887 created "2018-05-17" @default.
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• W2802674887 date "2018-05-07" @default.
• W2802674887 modified "2023-10-17" @default.
• W2802674887 title "Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation" @default.
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• W2802674887 doi "https://doi.org/10.3389/fimmu.2018.00916" @default.
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