Investigating alterations associated with heat stress and the recovery of the intestinal barrier using IPEC-J2 as an intestinal epithelial porcine cell model.

Heat stress (HS) is a growing concern due to global warming, especially for species with limited thermoregulatory capacity. The mechanisms underlying HS effects on digestive functions remain to be elucidated. The present study investigated the impacts of HS (41 °C for 5 days) followed by a recovery phase (37 °C for 5 days) to simulate a heatwave, on porcine intestinal epithelial cells (IPEC-J2) by focusing on barrier defense mechanisms. During HS, cell viability and apoptosis, permeability, tight junction (TJ) proteins, mucin expression and oxidative stress balance were affected as compared to cells staying at 37 °C (TN)(P < 0.05). During the recovery phase, most of the HS-induced alterations were rapidly reversed: apoptosis rates were normalized, paracellular permeability returned to Thermo Neutral (TN) levels, and TJ proteins (ZO-1 and occludin) localization were restored. Antioxidant enzyme abundance and Nrf2 levels were also similar to those in TN cells, but HSP70 abundance decreased below TN levels. Altogether, this study reveals specific adaptive intestinal mechanisms to HS, contributing to partial resilience of the digestive functions under heatwaves.