TRPV6 Deficiency Attenuates Stress and Corticosterone-Mediated Exacerbation of Alcohol-Induced Gut Barrier Dysfunction and Systemic Inflammation

Here, we report that a member of the Transient Receptor Potential ion channel subfamily, TRPV6, plays an essential role in stressand corticosterone-induced gut and liver injury. In this manuscript, we present data to demonstrate that: 1. Corticosterone andstress-induced intestinal epithelial tight junction disruption, mucosal barrier dysfunction, endotoxemia, systemic inflammation,and liver damage by a TRPV6-dependent mechanism. 2. TRPV6 is required for corticosterone and CRS-mediated potentiation ofalcohol-induced gut barrier dysfunction, endotoxemia, and liver damage. 3. TRPV6 also plays a role in corticosterone, stress, andalcohol-induced dysbiosis of gut microbiota. This study identifies TRPV6 as a potential therapeutic target in treating stress andalcohol-associated gut barrier dysfunction and systemic injuries.