Food allergy (FA) is an aberrant immune response triggered by the ingestion of a food antigen. Ovalbumin (OVA)-sensitized and challenged BALB/c mice were orally administered heat-killed (HK)-L. paracasei JY56. In this work, HK-L. paracasei JY56 alleviated the FA-induced decrease in body weight and rectal temperature and reduced the allergy score. Serum analysis showed that HK-L. paracasei JY56 reduced the levels of specific antibodies (OVA-sIgE and OVA-sIgG) and allergic mediators (histamine and mast cell protease) in FA mice. In addition, HK-L. paracasei JY56 also could alleviate OVA-induced FA by suppressing Th2 and Th17-type immune responses, which was evidenced by the regulation of splenic lymphocyte subpopulations and associated cytokine secretion. Moreover, jejunal histological analysis and intestinal barrier function related gene expression measurement were performed to verify the intestinal barrier repair of HK-L. paracasei JY56. Meanwhile, the TLR4/NF-κB inflammatory pathway activation was inhibited by HK-L. paracasei JY56 at gene and protein levels. Finally, HK-L. paracasei JY56 was performed to modulate the gut microbiota structure and increase the levels of short-chain fatty acids. In conclusion, HK-L. paracasei JY56 could alleviate OVA-induced FA in multiple ways, and this study provides a theoretical basis for the application of inactivated probiotics in functional foods for FA.

Reduced immunity can harm the health of the organism, and nowadays, improving immunity is getting more and more attention, so the nutrients with immune boosting function (acerola cherry, taurine, zinc gluconate, and lactoferrin) are compounded in the best ratio to develop a nutritional formula food, and evaluated by cellular immunity, humoral immunity, non-specific immunity. In this study, an immunocompromised mice model was established using cyclophosphamide (CTX), the ability and difference of different components to enhance the immunity of mice were determined by the gavage of different components. The results showed that the nutritional formula food could recover the body weight of immunocompromised mice, promote the development of immune organs in immunocompromised mice, enhance the delayed-type hypersensitivity (DTH) response, the ability to produce serum hemolysin and the phagocytosis of monocytes in immunocompromised mice, and increase the levels of immunoglobulin A (IgA), IgG and IgM in the serum of immunocompromised mice. It has proved that this nutritional formula food (containing acerola cherry, taurine, zinc gluconate, and lactoferrin) has synergistic effect and can work together on humoral immunity, cellular immunity and non-specific immunity to improve the immune resistance of mice, and has promising application.

Branched-chain fatty acids (BCFAs) are new bioactive fatty acids with anti-inflammatory properties. However, the role of BCFAs in alleviating ulcerative colitis has not been clarified. Herein, we evaluated the protective effect of BCFAs from goat milk in mice with colitis induced using dextran sodium sulfate and explore the corresponding mechanism. These results show that BCFAs extracted from goat milk can significantly alleviate weight loss in mice, and reduce the disease activity index and the activity of myeloperoxidase while increasing the content of antioxidant enzymes in colon tissue and reducing the oxidation stress response. These data also show that BCFAs can down-regulate the gene and protein expression of the Toll-like receptor 4 (TLR4)/ nuclear factor kappa-B p65 (NF-κB p65)/NOD-like receptor thermal protein domain associated protein 3 (NLRP3) signaling pathway, and at the same time significantly reduce the expression of pro-inflammatory factors Tumor Necrosis Factor Alpha (TNF-α), Interleukin 1β (IL-1β), and Interleukin 18 (IL-18) in colon tissue, and significantly increase the expression of the anti-inflammatory factor Interleukin 10 (IL-10). In conclusion, these results demonstrated that BCFAs in goat milk exerted effects on colitis-related inflammatory cytokines and inhibited inflammation by inducing the TLR4/NF-κB/NLRP3 pathway to alleviate dextran sodium sulfate (DSS)-induced ulcerative colitis. This study provides evidence for the potential of BCFAs as bioactive fatty acids in food products and to ameliorate ulcerative colitis development in mice.