Fructooligosaccharides protect against OVA-induced food allergy in mice by regulating the Th17/Treg cell balance using tryptophan metabolites.

Fructooligosaccharides (FOS) can change gut microbiota composition and play a protective role in food allergy (FA). Furthermore, the protective mechanism of FOS against FA is unclear. In this study, intestinal flora and tryptophan (Trp) metabolites were investigated in a mouse model with FA supplemented with FOS. Meanwhile, we injected aryl hydrocarbon receptor antagonists (AhR-A) into a mouse model of FA supplemented with FOS to investigate whether T helper cell (Th) 17/regulatory T (Treg) cell balance was affected. Our research studies showed that dietary intake of FOS provided moderate protection from the intestinal inflammation induced by ovalbumin (OVA). This protective effect disappeared in AhR-A mice. The OVA mice manifestations had significantly lower bacterial richness, when compared to the normal control (NC) mice. Among fecal bacteria, the abundance of Akkermansiaceae (family level) and Verrucomicrobia (phylum level) increased and Ruminococcacere (phylum level) decreased in the feces of allergic mice. These changes were reversed by FOS treatment. FOS modulated the gut microbiome profiles that were altered in OVA mice, which showed an increase in the abundance of Ruminococcacere (phylum level) and a decrease in the abundance of Akkermansiaceae (family level) and Verrucomicrobia (phylum level). Liquid chromatography/tandem mass spectrometry (LC-MS/MS) analysis of Trp metabolites showed significant reductions in the level of kynurenine (kyn) in the serum of OVA mice, as compared to NC and FOS mice. Conversely, the levels of Trp and 5-hydroxytryptamine (5-HT) were significantly increased in OVA mice. Correlation analysis revealed a negative relationship between the relative abundance of Verrucomicrobiae (class level) and Akkermansiaceae (family level) with kyn, and a positive relationship with 5-HT. FOS significantly reduced interleukin-17A (IL-17A) and retinoic acid-associated nuclear orphan receptor-γt (RORγt) in FOS mice but not in AhR-A mice. FOS increased the level of interleukin-10 (IL-10) and Forkhead box P3 (Foxp3) in FOS mice but not in AhR-A mice. These findings suggest that FOS ameliorates allergic symptoms and impacts Th17/Treg balance in mice by modulating the gut microbiota composition and Trp metabolites. FOS may serve as an effective tool for the treatment of FA by regulating immune and gut microbiota.

Xianyu decoction attenuates the inflammatory response of human lung bronchial epithelial cell.

BACKGROUND: Xianyu decoction (XD), a Chinese experience recipe, shows inhibitory effects on lung cancer. However, the potential functions of XD on pneumonia were unknown. This study aimed to investigate the effect of XD on inflammatory response of childhood pneumonia. METHODS: Human lung bronchial epithelial cell line BEAS-2B was cultured in different doses of LPS with or without XD treatment. The expression of miR-15a and IKBKB were altered by transfection assay. RT-PCR and western blot were used to evaluate the effects of XD and miR-15a mimic/inhibitor on the expression levels of miR-15a, IKBKB, p65 and IκBα. ELISA was used to determine the levels of CRP, IL-6 and IL-8. RESULTS: High expression of miR-15a was observed in serum and cell model of pneumonia. miR-15a promoted the expression of inflammatory cytokines IL-6, IL-8, CRP and IKBKB in vitro. XD treatment downregulated the level of miR-15a in pneumonia children. In addition, XD reduced the expression of inflammatory cytokines and the phosphorylation levels of p65 and IκBα by inhibition of miR-15a and IKBKB expression in LPS-stimulated BEAS-2B cells. CONCLUSION: XD downregulated the level of miR-15a in serum of pneumonia children. Additionally, XD inhibited inflammatory response in LPS-stimulated BEAS-2B cells possibly by blocking IKBKB/NF-κB signal pathway which was regulated by miR-15a.