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Objective: To investigate the effect of Bifidobacterium animalis subsp. lactis XLTG11 (XLTG11) on immune function and intestinal flora in cyclophosphamide (CTX)-immunosuppressed mice. Methods: Altogether 60 mice were randomly divided into five groups: blank, model, low-dose, medium-dose and high-dose XLTG11 groups. The blank group was injected intraperitoneally with normal saline from day 1 to 3, and the other groups 100 μL of CTX solution (40 mg/kg) to establish an immunocompromised mouse model. From day 4 to 30, the low-, medium- and high-dose XLTG11 groups were given 0.2 mL of XLTG11 suspensions at doses of 2.5 × 106, 2.5 × 107 and 2.5 × 108 CFU/animal, respectively, and both blank and model groups 0.2 mL of normal saline/animal. Body mass, immune organ index, delayed-type metamorphosis, proliferation of splenic lymphocytes, T-lymphocyte subpopulation, natural killer (NK) cell activity, phagocytic activity of peritoneal macrophages, cytokine levels, intestinal flora structure, and short-chain fatty acids (SCFA) were detected in each group of mice. Results: XLTG11 increased the immune organ index, foot-plantar thickness, splenic lymphocyte proliferation, T lymphocyte subsets CD4+ and CD8+, NK cell activity and macrophage phagocytosis activity, and cellular immune factors (interleukin (IL)-6, IL-10, IL-1β and interferon (IFN)-γ) in immunosuppressed mice. In addition, XLTG11 alleviated intestinal tissue damage caused by CTX, regulated the intestinal flora and increased intestinal SCFA (acetic, propionic and butyric acid) levels. Conclusion: XLTG11 could significantly enhance the immune function and regulate the intestinal flora of mice.

Breast milk is the safest and most perfect natural food for infant growth and development. As one of the most important components in breast milk, the milk fat globule membrane (MFGM) is a 3-layer membrane structure surrounding milk fat globules (MFG). This unique structure not only maintains the stability of milk but also plays an important role in the digestive and metabolic processes of infants. In this article, we introduce the reader to the composition and structural specificity of MFGM, review the sequential digestion of MFGM depending on several enzymes in the mouth, stomach and intestine of healthy infants, and elaborate on the interaction mechanism between MFGM and various enzymes, in order to provide a reference for relevant studies.

BackgroundB lymphocytes have multifaceted functions in the tumour microenvironment, and their prognostic role in human cancers is controversial. Here we aimed to identify tumour microenvironmental factors that influence the prognostic effects of B cells.MethodsWe conducted a gene expression analysis of 3585 patients for whom the clinical outcome information was available. We further investigated the clinical relevance for predicting immunotherapy response.ResultsWe identified a novel B cell-related gene (BCR) signature consisting of nine cytokine signalling genes whose high expression could diminish the beneficial impact of B cells on patient prognosis. In triple-negative breast cancer, higher B cell abundance was associated with favourable survival only when the BCR signature was low (HR = 0.68, p = 0.0046). By contrast, B cell abundance had no impact on prognosis when the BCR signature was high (HR = 0.93, p = 0.80). This pattern was consistently observed across multiple cancer types including lung, colorectal, and melanoma. Further, the BCR signature predicted response to immune checkpoint blockade in metastatic melanoma and compared favourably with the established markers.ConclusionsThe prognostic impact of tumour-infiltrating B cells depends on the status of cytokine signalling genes, which together could predict response to cancer immunotherapy.

The primary criterion for selecting probiotics having application potential is their adhesion capability to the host intestinal mucosa. The adhesion mechanism of probiotics is affected by many factors such as adhesins. Probiotics with high adhesion capability has a long intestinal residence time, contributing to their intestinal colonization in animals and stimulating intestinal barrier and metabolic functions, in turn maintaining the health of organisms. In addition, they can exert antagonistic effects against pathogens to protect intestinal health via many mechanisms such as producing antimicrobials and decreasing the adhesion capacity of pathogens and competitive binding sites. In this article, the adhesion mechanism of probiotics is reviewed, and a comprehensive overview of the state of the art in research on the adhesion characteristics and antagonistic activity against pathogens of probiotics is given.

Objective: To investigate the relieving effect of Bifidobacterium animalis subsp. lactis XLTG11 on antibiotic-associated diarrhea (AAD) in mice using clindamycin-induced AAD model. Methods: Forty-eight 6-week-old C57BL/6N male mice were randomly divided into four groups: normal control, model, low-dose and high-dose XLTG11. All mice except for the control group were administered with clindamycin orally daily for 14 days to induce AAD, The low-dose and high-dose groups were given 0.2 mL of the bacterial suspensions with viable count of 5 × 106 and 1 × 107 CFU, respectively. Body mass gain, cecum mass, fecal water content and fecal consistency score were measured. The levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-1β, and IL-10 in cecum tissue and the serum levels of lipopolysaccharide (LPS) and D-lactic acid were determined. The gut microbiota composition and the fecal contents of short-chain fatty acids were detected. The expression levels of genes related to the intestinal barrier and the nuclear factor kappa-B (NF-kB) pathway were determined. Results: The high dose of Bifidobacterium animalis subsp. lactis XLTG11 significantly increased the body mass gain and anti-inflammatory cytokine levels (P < 0.05), and significantly decreased cecum mass, fecal water content, fecal consistency score and proinflammatory cytokine levels in the mouse model mice of AAD. Moreover, it significantly up-regulated the gene expression levels of ZO-1, occludin, claudin-1 and MUC2, regulated the composition of the gut microbiota, evidently increased the fecal contents of acetate, propanoate, and butanoate, and significantly down-regulated the expression levels of genes related to the Toll like receptor 4 (TLR4), myeloid differentiation factor (MYD88) and NF-κB signaling pathway. Conclusion: Bifidobacterium animalis subsp. lactis XLTG11 can effectively alleviate AAD symptoms in mice by regulating cytokines and the gut microbiota, increasing fecal short-chain fatty acid contents, increasing the expression levels of intestinal barrier related genes and inhibiting the activation of the TLR4/MyD88/NF-kB signaling pathway.

Milk protein sensitivity is a major challenge in infant feeding, especially for infants who cannot receive adequate breastfeeding. Hydrolyzed milk protein is a mainstream way to address this difficulty. The aim of this study was to assess the effect of differences in whey protein concentrate (WPC) source and the degree of hydrolysis on blocking allergy and to analyze the possible mechanisms by which hydrolyzed infant formula (IF) blocks allergy through colony‐metabolism–immunity response. First, we prepared six groups of goat's milk IF with unhydrolyzed, partially, and extensively hydrolyzed WPC, which come from cow's milk WPC and goat's milk WPC. Subsequently, we evaluated their effects on allergy. The results showed that the hydrolyzed IF improved the allergic characteristics of mice, including low levels of total immunoglobulin E (IgE), specific IgE, histamine, and mucosal mast cell protease‐1 (mMCP‐1). Furthermore, the hydrolyzed IF promoted the immune response of T helper 1 (Th1) and regulatory T (Treg) cells by enhancing the messenger RNA (mRNA) expression of T‐box transcription factor 21 (T‐bet) and forkhead box protein P3 (Foxp3), which in turn suppressed the T helper 2 (Th2) overexpressed immune response in allergy (GATA‐binding protein 3 (GATA‐3) and retinoic‐acid‐receptor‐related orphan receptor gamma t (RORγt) mRNA expression, as well as interleukin 4 (IL‐4) and interleukin 5 (IL‐5) levels). Hydrolyzed IF promoted an increase in beneficial gut microbe Lactobacillus and Alistipes, which in turn promoted an increase in intestinal butyrate levels. The beneficial bacteria and their metabolized butyrate may have suppressed the abundance of the allergy‐characterizing bacterium Rikenellaceae‐RC9‐gut‐group. The final result we obtained was that for both cow's milk WPC and goat's milk WPC, at similar levels of hydrolysis, they did not bring about a significant effect on allergy symptoms. The hydrolyzed IF improved the allergic characteristics of mice, the deeper the degree of hydrolysis of WPC, the more obvious the effect of reducing allergic symptoms in model mice. [ABSTRACT FROM AUTHOR]

Human milk oligosaccharides (HMOs) are an evolutionarily significant advantage bestowed by mothers for facilitating the development of the infant's gut microbiota. They can avoid absorption in the stomach and small intestine, reaching the colon successfully, where they engage in close interactions with gut microbes. This process also enables HMOs to exert additional prebiotic effects, including regulating the mucus layer, promoting physical growth and brain development, as well as preventing and mitigating conditions such as NEC, allergies, and diarrhea. Here, we comprehensively review the primary ways by which gut microbiota, including Bifidobacteria and other genera, utilize HMOs, and we classify them into five central pathways. Furthermore, we emphasize the metabolic benefits of bacteria consuming HMOs, particularly the recently identified intrinsic link between HMOs and the metabolic conversion of tryptophan to indole and its derivatives. We also examine the extensive probiotic roles of HMOs and their recent research advancements, specifically concentrating on the unsummarized role of HMOs in regulating the mucus layer, where their interaction with the gut microbiota becomes crucial. Additionally, we delve into the principal tools used for functional mining of new HMOs. In conclusion, our study presents a thorough analysis of the interaction mechanism between HMOs and gut microbiota, emphasizing the cooperative utilization of HMOs by gut microbiota, and provides an overview of the subsequent probiotic effects of this interaction. This review provides new insights into the interaction of HMOs with the gut microbiota, which will inform the mechanisms by which HMOs function. [ABSTRACT FROM AUTHOR]