IL-13 deficiency exacerbates lung damage and impairs epithelial-derived type 2 molecules during nematode infection

摘要: IL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as infection with nematodes. However, dysregulation of can also contribute to the pathogenesis atopic and fibrotic diseases allergic asthma. Matrix remodelling is an important component repair processes in lung but hallmark chronic conditions involving fibrosis. Hence, understanding tissue has clinical implications. Since shares receptors signalling pathways IL-4, disentangling relative contributions these cytokines been challenging. Additionally, little known about singular following acute injury. In this study, we used Nippostrongylus brasiliensis model damage repair, comparing between WT IL-13-deficient mice, which IL-4 intact. Importantly, found that played critical limiting injury haemorrhaging infection. Through proteomic transcriptomic profiling, identified IL-13-dependent changes matrix associated regulators. We further showed required for induction epithelial-derived effector molecules RELM-alpha surfactant protein D. Pathway analyses predicted was heavily involved cellular stress regulation epithelial cell differentiation by suppression Foxa2 pathways. Thus, propose tissue-protective functions regulates immunity setting.