IL-17A, But Not IL-17F, Is Indispensable for Airway Vascular Remodeling Induced by Exaggerated Th17 Cell Responses in Prolonged Ovalbumin-Challenged Mice

摘要: We previously demonstrated an essential role of Th17 cells in excessive mucous secretion and airway smooth muscle proliferation a prolonged OVA-challenged C57BL/6 mouse model. However, the impact vascular remodeling, another characteristic feature remodeling asthma, remains elusive. This issue was further investigated this study. The time-course experiments showed that progressively increasing levels IL-17A (not IL-17F) lungs allergen-challenged mice were positively correlated with microvessel density peribronchial tissues. In addition, exaggerated model exacerbated by administration or adoptive transfer cells. effect dramatically alleviated anti-IL-17A Ab, but not anti-IL-17F Ab. Boyden chamber assays indicated accelerates endothelial progenitor cell (EPC) migration. Furthermore, EPC accumulation airways allergen-exposed after eliminated blockade IL-17A. found promoted tubule-like formation rather than pulmonary microvascular endothelia (PMVECs) vitro. induced PMVEC tube via PI3K/AKT1 pathway, suppression PI3K pathway markedly reduced structures. Collectively, our results indicate contribute to asthma mediating chemotaxis, as well formation, IL-17F.