Bacillus amyloliquefaciens SC06 alleviates LPS-induced intestinal damage by inhibiting endoplasmic reticulum stress and mitochondrial dysfunction in piglets

Abstract

Endoplasmic reticulum stress (ERS) and mitochondrial dysfunction play an important role in the pathogenesis of intestinal diseases. Our studies investigated the effects of Bacillus amyloliquefaciens SC06 on jejunal mitochondria and ER in piglets under the LPS-induced intestinal injury model. Eighteen piglets (male, 21 days old) were randomly assigned to three treatments: CON (basal diet), LPS (basal diet +100 μg/kg LPS), and SC06 + LPS (basal diet +1 × 10⁸ cfu/kg SC06 + 100 μg/kg LPS). Compared to the LPS group, administration of SC06 improved jejunal morphology and barrier function. In addition, SC06 reduced reactive oxygen species (ROS) and MDA generation in the jejunum by activating the Nrf2/keap1 pathway, which increased the activity of CAT, GSH and SOD in LPS-challenged pigs. In addition, SC06 reduced LPS-induced mitochondrial dysfunction and ERS as evidenced by a decrease in ROS, an improvement in mitochondrial membrane potential and an increase in adenosine triphosphate levels. The results of in vitro IPEC-J2 cell experiments also indicate that SC06 can reduce LPS-induced oxidative stress, mitochondrial dysfunction, ERS, and intestinal barrier function damage by activating the Nrf2/keap1 signaling pathway. Finally, treatment with the Nrf2-specific inhibitor ML-385 inhibited the upregulated effect of SC06 on antioxidant capacity and intestinal barrier function in IPEC-J2 cells. In conclusion, SC06 ameliorated intestinal damage and mitochondrial dysfunction and attenuated endoplasmic reticulum stress via activation of the Nrf2/keap1 signaling pathway in LPS-challenged piglets.

Keywords: Bacillus amyloliquefaciens SC06; Endoplasmic reticulum; Intestinal injury; Mitochondria; Nrf2/keap1 signal pathway; Oxidative stress; Piglets.