”Effects of IL-22 Depletion on Airway Remodeling and Bronchus-Associated Lymphoid Tissue in Neutrophilic asthma 9191

Abstract Description Background Severe allergic asthma is a chronic inflammatory airway disease. T2 low asthma is associated with bronchial remodelling, neutrophil recruitment in the lung, and Th17 cytokine production. Among Th17 cytokines, IL-22 is involved in neutrophil recruitment, tissue remodelling and is induced in response to infectious agents, some involved in the exacerbation of asthma. The aim of this study was to determine the role of IL-22 in an asthma model by using IL-22 deficient mice. Materials and Methods The role of IL-22 was investigated in a model of dog allergen-induced chronic asthma, using Wild-Type and IL22 deficient mice. Asthma parameters were evaluated including airway resistances, bronchoalveolar lavage (BAL) cell counts, lung cytokine expression, and bronchial remodelling. Induced Bronchus associated lymphoid tissue (iBALT) was assessed by immunostaining against T cells, B cells and follicular dendritic cells (FdC). Results Dog-sensitized/challenged IL22 deficient mice exhibited decreased total cell and neutrophil BAL recruitment, abolished airway hyperresponsiveness compared with wild-type mice. The number of iBALT was also decreased together with loss of FdC. However, there was no modification in lung cytokine expression. In contrast, a strong decrease in the parameters associated with bronchial remodelling was observed. Conclusions These results suggest that therapies targeting IL-22 may be of interest in neutrophilic T2 low asthma with strong bronchial remodelling. Topic Categories Immediate Hypersensitivity, Asthma, and Allergic Responses (HYP)