Determinate the effects of Arabic gum and Lactobacillus acidophilus on the gut microbiota ALPK1/NFKB/NLRP6 and NLRP2 signaling pathway and virulence gene profile in rats with Campylobacter jejuni exosome application

Campylobacter jejuni (CJ), a major cause of bacterial gastroenteritis, employs exosomes to disseminate virulence factors and disrupt host immune homeostasis. This study investigated the therapeutic potential of Arabic Gum (AZ) and Lactobacillus acidophilus (LA), individually and in combination, against CJ exosome-induced intestinal injury in rats, with emphasis on inflammasome-related signaling and microbiota modulation. Rats received AZ, LA, or both following CJ exosome exposure. Molecular analyses, histopathology, and microbiome sequencing were performed to elucidate mechanistic responses. CJ exosomes activated key virulence pathways and triggered pronounced inflammatory signaling characterized by alpha kinase 1 (ALPK1), Nuclear Factor Kappa B (NF-κB), and NOD-like Receptor Pyrin (NLRP) upregulation, accompanied by epithelial injury and dysbiosis. Treatment with AZ or LA alone attenuated inflammasome activation and partially restored immune and microbial balance. Notably, the combined treatment produced a synergistic effect, effectively suppressing ALPK1/NF-κB/NLRP signaling and reestablishing a more physiologic microbial community structure. These improvements were associated with reductions in pro-inflammatory cytokines and markers of tissue damage, as well as substantial recovery in intestinal, hepatic, and splenic architecture. Overall, AZ and LA significantly mitigated CJ exosome-mediated pathology, with the combined therapy demonstrating superior efficacy. The findings suggest that co-administration of AZ and LA may offer a promising dual-modal strategy to counteract CJ-induced inflammatory and microbial disturbances, potentially supporting future therapeutic approaches targeting exosome-mediated pathogenesis. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2026.