This study investigated the effects of TMEM16A on intestinal epithelial barrier function in vitro using LPS-induced cell damage in IEC-6 cells. LPS significantly increased TMEM16A expression, potentially via NF-κB and Th1/Th2 cytokines. Low-dose LPS caused tight junction dysregulation, while high-dose LPS induced apoptosis-dependent barrier dysfunction. TMEM16A aggravated barrier dysfunction with low-dose LPS by activating ERK1/MLCK signaling but protected against it with high-dose LPS by activating ERK/Bcl-2/Bax signaling. TMEM16A thus plays a dual role in LPS-induced epithelial dysfunction.
