Dataset Information

Qi-Deficiency Related Increases in Disease Susceptibility Are Potentially Mediated by the Intestinal Microbiota.

ABSTRACT: Qi-deficiency (QX) is thought to promote the body's susceptibility to disease, but the underlying mechanism through which this occurs is not clear. We surveyed the traditional Chinese medicine constitution (TCMC) of healthy college students to identify those that were PH (balanced TCMC constitution) and QX (unbalanced TCMC constitution). We then used high-throughput sequencing of the 16SrRNA V3-4 region in fecal microbiota samples to identify differences between those obtained from PH and QX individuals. Our results demonstrated that the alpha diversity of QX samples was significantly lower than that of PH samples (p < 0.05) and that beta diversity was remarkably different in QX and PH samples. Four and 122 bacterial taxa were significantly overrepresented in QX and PH groups, respectively. The genera Sphingobium, Clostridium, and Comamonas were enriched in the QX group and had a certain pathogenic role. The QX group also showed a statistically significant lack of probiotics and anti-inflammatory bacteria such as Bifidobacterium and Bdellovibrio. The functional potential of QX bacterial taxa was reduced in fatty acid metabolism and butanoate metabolism. We contend that the imbalanced intestinal microbiota in QX and the following functional changes in metabolism influence immunity and energy metabolism, which could increase susceptibility to disease.

SUBMITTER: Ma K

PROVIDER: S-EPMC6218746 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Qi-Deficiency Related Increases in Disease Susceptibility Are Potentially Mediated by the Intestinal Microbiota.

Ma Ke K Chen Jieyu J Kuang Liuyan L Bi Jianlu J Cheng Jingru J Li Fei F Sun Xiaomin X Nie Xiaoli X Liu Yanyan Y Luo Ren R Zhao Xiaoshan X

Evidence-based complementary and alternative medicine : eCAM 20181023

Qi-deficiency (QX) is thought to promote the body's susceptibility to disease, but the underlying mechanism through which this occurs is not clear. We surveyed the traditional Chinese medicine constitution (TCMC) of healthy college students to identify those that were PH (balanced TCMC constitution) and QX (unbalanced TCMC constitution). We then used high-throughput sequencing of the 16SrRNA V3-4 region in fecal microbiota samples to identify differences between those obtained from PH and QX ind ...[more]

PMID: 30425748

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Project description:Background and aimsPrevious study disclosed Fucosyltransferase 2 (Fut2) gene as a IBD risk locus. This study aimed to explore the mechanism of Fut2 in IBD susceptibility and to propose a new strategy for the treatment of IBD.MethodsIntestinal epithelium-specific Fut2 knockout (Fut2△IEC) mice was used. Colitis was induced by dextran sulfate sodium (DSS). The composition and diversity of gut microbiota were assessed via 16S rRNA analysis and the metabolomic findings was obtained from mice feces via metabolite profiling. The fecal microbiota transplantation (FMT) experiment was performed to confirm the association of gut microbiota and LPC. WT mice were treated with Lysophosphatidylcholine (LPC) to verify its impact on colitis.ResultsThe expression of Fut2 and α-1,2-fucosylation in colonic tissues were decreased in patients with UC (UC vs. control, P = 0.036) and CD (CD vs. control, P = 0.031). When treated with DSS, in comparison to WT mice, more severe intestinal inflammation and destructive barrier functions in Fut2△IEC mice was noted. Lower gut microbiota diversity was observed in Fut2△IEC mice compared with WT mice (p < 0.001). When exposed to DSS, gut bacterial diversity and composition altered obviously in Fut2△IEC mice and the fecal concentration of LPC was increased. FMT experiment revealed that mice received the fecal microbiota from Fut2△IEC mice exhibited more severe colitis and higher fecal LPC concentration. Correlation analysis showed that the concentration of LPC was positively correlated with four bacteria-Escherichia, Bilophila, Enterorhabdus and Gordonibacter. Furthermore, LPC was proved to promote the release of pro-inflammatory cytokines and damage epithelial barrier in vitro and in vivo.ConclusionFut2 and α-1,2-fucosylation in colon were decreased not only in CD but also in UC patients. Gut microbiota in Fut2△IEC mice is altered structurally and functionally, promoting generation of LPC which was proved to promote inflammation and damage epithelial barrier.

Project description:Alcohol use in persons living with HIV (PLWH) worsens the severity of bacterial pneumonia. However, the exact mechanism(s) by which this occurs remain ill-defined. We hypothesized that alcohol in the setting of HIV infection decreases Streptococcus pneumoniae clearance from the lung through mechanisms mediated by the gut microbiota. Humanized BLT (bone marrow, liver, thymus) mice were infected with 1 × 104 TCID50 of HIV (BAL and JRCSF strains) via intraperitoneal (i.p.) injection. One week post-HIV infection, animals were switched to a Lieber-DeCarli 5% ethanol diet or an isocaloric control diet for 10 days. Alcohol-fed animals were also given two binges of 2 g/kg ethanol on days 5 and 10. Feces were also collected, banked, and the community structures were analyzed. Mice were then infected with 1 × 105 CFU (colony-forming units) of S. pneumoniae and were sacrificed 48 h later. HIV-infected mice had viral loads of ∼2 × 104 copies/mL of blood 1 week post-infection, and exhibited an ∼57% decrease in the number of circulating CD4+ T cells at the time of sacrifice. Fecal microbial community structure was significantly different in each of the feeding groups, as well as with HIV infection. Alcohol-fed mice had a significantly higher burden of S. pneumoniae 48 h post-infection, regardless of HIV status. In follow-up experiments, female C57BL/6 mice were treated with a cocktail of antibiotics daily for 2 weeks and recolonized by gavage with intestinal microbiota from HIV+ ethanol-fed, HIV+ pair-fed, HIV- ethanol-fed, or HIV- pair-fed mice. Recolonized mice were then infected with S. pneumoniae and were sacrificed 48 h later. The intestinal microbiota from alcohol-fed mice (regardless of HIV status) significantly impaired clearance of S. pneumoniae. Collectively, these data indicate that alcohol feeding, as well as alcohol-associated intestinal dysbiosis, compromise pulmonary host defenses against pneumococcal pneumonia. Determining whether HIV infection acts synergistically with alcohol use in impairing pulmonary host defenses will require additional study.

Dataset Information

Qi-Deficiency Related Increases in Disease Susceptibility Are Potentially Mediated by the Intestinal Microbiota.

Publications

Qi-Deficiency Related Increases in Disease Susceptibility Are Potentially Mediated by the Intestinal Microbiota.

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