Bacteria from porcine colon regulate cytokine and transcription factor expression in the gut of the mouse model of colitis

Abstract:

[Background] Microorganisms in the mammalian digestive tract are important for maintaining gut homeostasis, while the regulatory role of gut bacteria in cytokine expression remains unclarified. [Objective] To compare the regulatory effects of different isolated from porcine intestinal tract on the expression of cytokines and transcription factors in the model of colitis. [Methods] Bacteria were isolated from the porcine colon, and the culture supernatant of each isolate was used to treat the Caco-2 cell model of lipopolysaccharide-induced inflammation. Furthermore, a mouse model of colitis was induced by dextran sodium sulfate (DSS) and then administrated with bacterial suspension by gavage. The gene expression of cytokines and transcription factors in Caco-2 cells and mouse colon tissue, the cell growth rate, and the mouse weight after bacterial treatment were determined. [Results] Six strains of bacteria were isolated from porcine colon, belonging to Enterococcus, Lactobacillus, Sharpea, and Mitsuokella. In the Caco-2 cell model of inflammation, Lactobacillus amylovorus LGM down-regulated the mRNA levels of interleukin (IL)-4 and IL-17 (P<0.05); Enterococcus cecorum LGM down-regulated the mRNA levels of T-box expressed in T cells (T-bet), forkhead box P3 (Foxp3), IL-17, and transforming growth factor-β (TGF-β) (P<0.05). In the mouse model of colitis, only L. amylovorus LGM alleviated the colon inflammation, restored the colon length, and up-regulated the mRNA levels of Foxp3, GATA Binding Protein 3 (GATA-3), and interferon-γ (IFN-γ) in the colon tissue (P<0.05). However, Mitsuokella jalaludinii LGM aggravated colon injury and up-regulated the mRNA level of interferon-γ in the tissue (P<0.05). [Conclusion] The bacterial isolates have different regulatory effects on porcine colitis, which is related to the regulation of cytokine gene expression. L. amylovorus LGM exerts an anti-inflammatory effect by up-regulating the expression of Foxp3 and GATA-3 in the colon.