Decreased Rac1 expression leads to upregulation of ILC2-related cytokines and aggravation of airway inflammation in allergic asthma mice

Allergic asthma is an inflammatory disease of the airways in which epithelial cells and group 2 innate lymphoid cells (ILC2s) are increasingly implicated. Recent findings suggest that airway epithelial undergo apoptosis after encountering environmental allergens then apoptotic cells are efficiently phagocytosed by airway epithelial cells via a Rac1-dependent manner and secrete anti-inflammatory cytokines. However, the expression level of Rac1 in asthma and its relationship with ILC2 polarization remains unclear. In this study, Rac1 and the ILC2s related cytokines in lung tissue, PBMC, BALF from the mice were measured, and the potential correlation between them was also analyzed. Our data showed that the expression levels of IL-25, IL-33, IL-5 and IL-13 mRNA were significantly increased while Rac1 level was decreased in asthmatic mice, and there was a negative correlation between the expression level of Rac1 and ILC2s related cytokines. After the Rac1 inhibitor EHT1864 was administrated, the expression levels of the ILC2s related cytokines were further increased, meanwhile the inflammatory was aggravated in asthmatic mice. These results suggested that the decreased Rac1 may contribute to the polarization of ILC2 and promote the development of asthma inflammation.