摘要：SummaryThe cornea is an avascular tissue for vision clarity. Alkali burn could cause severe traumatic damage on the cornea with inflammation and neovascularization (NV), leading to vision reduction and blindness. Mechanisms underlying corneal inflammation and NV are not as clear. We previously reported that Zeb1 is an important factor in corneal NV, and we sought to clarify whether it is also involved in regulation of corneal inflammation. We analyzed the alkali burn-induced corneal inflammation and wound healing in both Zeb1+/+and Zeb1−/+littermates through a multidisciplinary approach. We provide evidence that Zeb1 forms a positive regulatory loop with Tgfb to regulate early corneal inflammation by maintenance of immune cell viability and mobility and later wound healing by activation of both Nf-κb and Tgfb-related Stat3 signaling pathways. We believe that ZEB1 is a potential therapeutic target, and inactivation of ZEB1 could be a strategy to treat severe corneal inflammation condition.Graphical abstractDisplay OmittedHighlights•Traumatic wound induces inflammation in the cornea, resulting in vision reduction•Zeb1 is a key factor to retain immune cell viability, mobility, and cytokine expression•Zeb1 regulates cytokine gene expression through both Nf-κb and Stat3 pathways•Inactivation of ZEB1 could be a strategy to treat severe corneal inflammation conditionOphthalmology; Biological sciences; Immunology
