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Effect of heat-killed Streptococcus thermophilus on type 2 diabetes rats.

ABSTRACT: Background and Aims:The link between gut microbiota and type 2 diabetes (T2D) has been addressed by numerous studies. Streptococcus thermophilus from fermented milk products, has been used as a probiotic in previous research. However, whether heat-killed S. thermophilus can improve the glycemic parameters of diabetic rats remains unanswered. In this study, we evaluated the effect of heat-killed S. thermophilus on T2D model rats and the potential mechanisms of the effect. Methods:Zucker diabetic fatty (ZDF) rats were used to generate a diabetic rat model induced by feeding a high-fat diet. Heat-killed S. thermophilus were orally administered to normal and diabetic rats for 12 weeks. Intestinal microbiota analysis, histology analysis, oral glucose tolerance test and measurement of inflammatory factors were performed. Results:We found that heat-killed S. thermophilus treatment reduced fasting blood glucose levels and alleviated glucose intolerance and total cholesterol in diabetic ZDF rats. Additionally, heat-killed S. thermophilus increased the interleukin 10 while reducing the levels of lipopolysaccharide, interleukin 6, and tumor necrosis factor-? in diabetic ZDF rats. The heat-killed S. thermophilus treatment can normalize the structure of the intestinal and colon mucosal layer of diabetic rats. The characteristics of the gut microbiota in heat-killed S. thermophilus-treated and control rats were similar. At the genus level, the abundances of beneficial bacteria, including Ruminococcaceae, Veillonella, Coprococcus, and Bamesiella, were all significantly elevated by heat-killed S. thermophilus treatment in ZDF diabetic rats. Conclusion:Our study supports the hypothesis that treatment with heat-killed S. thermophilus could effectively improve glycemic parameters in T2D model rats. In addition, the potential mechanisms underlying the protection maybe include changing the composition of gut microbiota, reinforcing the intestinal epithelial barrier and the immunity of the intestinal mucosa, decreasing the level of inflammation, and then reducing the insulin resistance.

SUBMITTER: Gao X

PROVIDER: S-EPMC6571132 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Effect of heat-killed <i>Streptococcus thermophilus</i> on type 2 diabetes rats.

Gao Xiangyang X Wang Fei F Zhao Peng P Zhang Rong R Zeng Qiang Q

PeerJ 20190613

<h4>Background and aims</h4>The link between gut microbiota and type 2 diabetes (T2D) has been addressed by numerous studies. <i>Streptococcus thermophilus</i> from fermented milk products, has been used as a probiotic in previous research. However, whether heat-killed <i>S. thermophilus</i> can improve the glycemic parameters of diabetic rats remains unanswered. In this study, we evaluated the effect of heat-killed <i>S. thermophilus</i> on T2D model rats and the potential mechanisms of the eff ...[more]

PMID: 31223540

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Project description:BackgroundDifferences in male vs. female immune responses are well-documented and have significant clinical implications. While the immunomodulatory effects of sex hormones are well established, the contributions of sex chromosome complement (XX vs. XY) and gut microbiome diversity on immune sexual dimorphisms have only recently become appreciated. Here we investigate the individual and collaborative influences of sex chromosome complements and gut microbiota on humoral immune activation.MethodsMale and female Four Core Genotype (FCG) mice were immunized with heat-killed Streptococcus pneumoniae (HKSP). Humoral immune responses were assessed, and X-linked immune-related gene expression was evaluated to explain the identified XX-dependent phenotype. The functional role of Kdm6a, an X-linked epigenetic regulatory gene of interest, was evaluated ex vivo using mitogen stimulation of B cells. Additional influences of the gut microbiome on sex chromosome-dependent B cell activation was also evaluated by antibiotically depleting gut microbiota prior to HKSP immunization. Reconstitution of the depleted microbiome with short-chain fatty acid (SCFA)-producing bacteria tested the impact of SCFAs on XX-dependent immune activation.ResultsXX mice exhibited higher HKSP-specific IgM-secreting B cells and plasma cell frequencies than XY mice, regardless of gonadal sex. Although Kdm6a was identified as an X-linked gene overexpressed in XX B cells, inhibition of its enzymatic activity did not affect mitogen-induced plasma cell differentiation or antibody production in a sex chromosome-dependent manner ex vivo. Enhanced humoral responses in XX vs. XY immunized FCG mice were eliminated after microbiome depletion, indicating that the microbiome contributes to the identified XX-dependent immune enhancement. Reconstituting microbiota-depleted mice with select SCFA-producing bacteria enhanced fecal SCFA concentrations and increased humoral responses in XX, but not XY, FCG mice. However, exposure to the SCFA propionate alone did not enhance mitogenic B cell stimulation in ex vivo studies.ConclusionsFCG mice have been used to assess sex hormone and sex chromosome complement influences on various sexually dimorphic traits. The current study indicates that the gut microbiome impacts humoral responses in an XX-dependent manner, suggesting that the collaborative influence of gut bacteria and other sex-specific factors should be considered when interpreting data aimed at delineating the mechanisms that promote sexual dimorphism.

Project description:BackgroundDifferences in male vs. female immune responses are well-documented and have significant clinical implications. While the immunomodulatory effects of sex hormones are well established, the contributions of sex chromosome complement (XX vs. XY) and gut microbiome diversity on immune sexual dimorphisms have only recently become appreciated. Here we investigate the individual and collaborative influences of sex chromosome complements and gut microbiome bacteria on humoral immune activation.MethodsSham-operated and gonadectomized male and female Four Core Genotype (FCG) mice were immunized with heat-killed Streptococcus pneumoniae (HKSP). Humoral immune responses were assessed, and X-linked immune-related gene expression was evaluated to explain the identified XX-dependent phenotypes. Ex vivo studies investigated the functional role of Kdm6a, an X-linked epigenetic regulatory gene of interest, in mitogenic B cell activation. Additionally, we examined whether gut microbiome communities, or their metabolites, differentially influence immune cell activation in a sex chromosome-dependent manner. Endogenous gut microbiomes were antibiotically depleted and reconstituted with select short-chain fatty acid (SCFA)-producing bacteria prior to HKSP immunization and immune responses assessed.ResultsXX mice exhibited higher HKSP-specific IgM-secreting B cells and plasma cell frequencies than XY mice, regardless of gonadal sex. Although Kdm6a was identified as an X-linked gene overexpressed in XX B cells, inhibition of its enzymatic activity did not affect mitogen-induced plasma cell differentiation or antibody production in a sex chromosome-dependent manner ex vivo. Enhanced humoral responses in XX vs. XY immunized FCG mice were eliminated after microbiome depletion, indicating that the microbiome contributes to the identified XX-dependent immune enhancement. Reconstituting microbiota-depleted mice with select SCFA-producing bacteria increased humoral responses in XX, but not XY, FCG mice. This XX-dependent enhancement appears to be independent of SCFA production in males, while female XX-dependent responses relied on SCFAs.ConclusionsFCG mice have been used to assess the influence of sex hormones and sex chromosome complements on various sexually dimorphic traits. The current study indicates that the gut microbiome impacts humoral responses in an XX-dependent manner, suggesting that the collaborative influence of gut bacteria and other sex-specific factors should be considered when interpreting data aimed at delineating the mechanisms that promote sexual dimorphism.

Dataset Information

Effect of heat-killed Streptococcus thermophilus on type 2 diabetes rats.

Publications

Effect of heat-killed <i>Streptococcus thermophilus</i> on type 2 diabetes rats.

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