LPS inactivation by a host lipase allows lung epithelial cell sensitization for allergic asthma

We report here that acyloxyacyl hydrolase (AOAH), a host lipase that degrades and inactivates LPS, renders mice more susceptible to house dust mite (HDM)–induced allergic asthma. Lung epithelial cells from Aoah–/– mice are refractory to HDM stimulation, decreasing dendritic cell activation and Th2 responses. Antibiotic treatment that diminished commensal LPS-producing bacteria normalized Aoah–/– responses to HDM, while giving LPS intrarectally ameliorated asthma. Aoah–/– mouse feces, plasma, and lungs contained more bioactive LPS than did those of Aoah+/+ mice. By inactivating commensal LPS, AOAH thus prevents desensitization of lung epithelial cells. An enzyme that prevents severe lung inflammation/injury in Gram-negative bacterial pneumonia has the seemingly paradoxical effect of predisposing to a Th2-mediated airway disease.

Source: The Journal of Experimental Medicine - September 3, 2018 Category: Internal Medicine Authors: Qian, G., Jiang, W., Zou, B., Feng, J., Cheng, X., Gu, J., Chu, T., Niu, C., He, R., Chu, Y., Lu, M. Tags: Mucosal Immunology Articles Source Type: research