Synergistic postbiotics from Bacillus pumilus SE5 attenuate soybean meal-induced enteritis in grouper by modulating intestinal microbiota and p38 MAPK/NF-κB/NLRP3 signaling.

High soybean meal (SBM) diets are increasingly used in aquaculture, but excessive SBM inclusion frequently triggers intestinal inflammation and growth retardation in fish. Peptidoglycan (PG) and lipoteichoic acid (LTA) extracted from Bacillus pumilus SE5 have previously been shown to regulate intestinal microbiota and enhance immunity in Epinephelus coioides, their efficacy against SBM-induced enteritis remains unclear. This study investigated the alleviation effects of PG and LTA (individually or combined) on SBM-induced enteritis. The trial set two control groups: LSM group (18% SBM) and HSM group (36.8% SBM); three reparative groups, in which after four weeks on 36.8% SBM feed, PG, LTA, or PG + LTA from B. pumilus SE5 were added (SPG, SLA, and SPL groups); and three preventive groups, in which PG, LTA, and PG + LTA were fed throughout the trial period (PG, LTA, and PLA groups). After eight weeks, the HSM group exhibited significantly reduced growth performance, disordered intestinal microbiota, elevated pro-inflammatory cytokines, nuclear factor kappa-B (NF-κB), and mitogen-activated protein kinase (MAPK) pathway-related genes, and impaired intestinal health compared to the LSM group. In contrast, compared with the HSM group, the preventive and reparative groups reversed the above phenomena, with the PLA group exhibiting the most significant effects. Notably, compared with the HSM group, the expression levels of NOD-like receptor family, pyrin domain-containing protein 3 (nlrp3), caspase 1, and gasdermin E (gsdme) genes were down-regulated in all preventive and reparative groups. Collectively, B. pumilus SE5-derived PG and LTA synergistically alleviated SBM-induced enteritis and the mechanisms might be correlated with the down-regulation of transcripts associated with the p38 MAPK/NF-κB/NLRP3 signaling pathways and modulation of intestinal microbiota.