Inflammatory bowel diseases (IBDs) are chronic, idiopathic, relapsing disorders of unclear etiology affecting millions of people worldwide. Aberrant interactions between the human microbiota and immune system in genetically susceptible populations underlie IBD pathogenesis. Despite extensive studies examining the involvement of the gut microbiota in IBD using culture-independent techniques, information is lacking regarding other human microbiome components relevant to IBD. Since accumulated knowledge has underscored the role of the oral microbiota in various systemic diseases, we hypothesized that dissonant oral microbial structure, composition, and function, and different community ecotypes are associated with IBD; and we explored potentially available oral indicators for predicting diseases. We examined the 16S rRNA V3–V4 region of salivary bacterial DNA from 54 ulcerative colitis (UC), 13 Crohn’s disease (CD), and 25 healthy individuals using Illumina sequencing. Distinctive sample clusters were driven by disease or health based on principal coordinate analysis (PCoA) of both the Operational Taxonomic Unit profile and Kyoto Encyclopedia of Genes and Genomes pathways. Comparisons of taxa abundances revealed enrichment of Streptococcaceae (Streptococcus) and Enterobacteriaceae in UC and Veillonellaceae (Veillonella) in CD, accompanied by depletion of Lachnospiraceae and [Prevotella] in UC and Neisseriaceae (Neisseria) and Haemophilus in CD, most of which have been demonstrated to exhibit the same variation tendencies in the gut of IBD patients. IBD-related oral microorganisms were associated with white blood cells, reduced basic metabolic processes, and increased biosynthesis and transport of substances facilitating oxidative stress and virulence. Furthermore, UC and CD communities showed robust sub-ecotypes that were not demographic or severity-specific, suggesting their value for future applications in precision medicine. Additionally, indicator species analysis revealed several genera indicative of UC and CD, which were confirmed in a longitudinal cohort. Collectively, this study demonstrates evident salivary dysbiosis and different ecotypes in IBD communities and provides an option for identifying at-risk populations, not only enhancing our understanding of the IBD microbiome apart from the gut but also offering a clinically useful strategy to track IBD as saliva can be sampled conveniently and non-invasively.

Halitosis is a common symptom mainly caused by microbial activities in the oral cavity. Here, we used 16S rRNA gene pyrosequencing and metagenomic sequencing to examine oral microbial compositions and their functional variations in children with halitosis. We found that the tongue coating of subjects with halitosis had greater bacterial richness than those of healthy subjects. The relative abundance and prevalence of Leptotrichia wadei and Peptostreptococcus stomatis were higher in tongue coating samples from children with halitosis than those from children without halitosis; Prevotella shahii had higher relative abundance and prevalence in saliva samples from children with halitosis. We present the first comprehensive evaluation of the co-occurrence networks of saliva and tongue coating communities under healthy and halitosis conditions, and investigated patterns of significant differences between these communities. Moreover, we observed that bacterial genes associated with responses to infectious diseases and terpenoid and polyketide metabolism were enriched in subjects with halitosis, but not in healthy subjects. Hydrogen sulphide (H2S)-related metabolic pathways suggested that there was higher microbial production and less usage of H2S in subjects with halitosis. Thus, the mechanism of halitosis was implied for the first time via metagenomic sequencing.

No abstract

Obesity has been recognized as a major risk factor for chronic kidney disease, but the underlying mechanism remains elusive. Here, we investigated the mechanism whereby long-term high-fat diet (HFD) feeding induces renal injury in mice. The C57BL/6 mice fed HFD for 16 weeks developed obesity, diabetes, and kidney dysfunction manifested by albuminuria and blood accumulation of BUN and creatinine. The HFD-fed kidney showed marked glomerular and tubular injuries, including prominent defects in the glomerular filtration barrier and increased tubular cell apoptosis. Mechanistically, HFD feeding markedly increased triglyceride and cholesterol contents in the kidney and activated lipogenic pathways for cholesterol and triglyceride synthesis. HFD feeding also increased oxidative stress and induced mitochondrial fission in tubular cells, thereby activating the pro-apoptotic pathway. In HK-2 and mesangial cell cultures, high glucose, fatty acid, and TNF-α combination was able to activate the lipogenic pathways, increase oxidative stress, promote mitochondrial fission, and activate the pro-apoptotic pathway, all of which could be attenuated by an inhibitor that depleted reactive oxygen species. Taken together, these observations suggest that long-term HFD feeding causes kidney injury at least in part as a result of tissue lipid accumulation, increased oxidative stress, and mitochondrial dysfunction, which promote excess programmed cell death.

BackgroundThe objective of this study was to characterize the oral microflora profile of primary Sjögren’s syndrome (pSS) patients, thereby revealing the connection between oral bacterial composition and dental caries, and to identify the “core microbiome” in the oral cavities of pSS patients and systemic healthy individuals by using a high-throughput sequencing technique.MethodsTwenty-two pSS patients and 23 healthy controls were enrolled in this study. Their clinical data and oral rinse samples were collected. The V3–V4 hypervariable regions of the bacterial 16S rRNA gene of samples were amplified and analyzed by high-throughput sequencing on the Illumina Miseq PE300 platform.ResultsBoth two groups were age- and sex-matched. There were significantly higher decayed, missing and filled teeth (DMFT) and decayed, missing and filled surfaces (DMFS) in the pSS group than in the control group (p < 0.01). Alpha diversity was depleted in pSS patients, compared with healthy controls (p < 0.01), while beta diversity between the two groups was not significantly different. Seven discriminative genera (LDA > 4) were found between the two groups in LEfSe (LDA Effect Size) analysis. The relative abundance of Veillonella in pSS patients was fourfold higher, while Actinomyces, Haemophilus, Neisseria, Rothia, Porphyromonas and Peptostreptococcus were significantly lower in pSS patients than in healthy controls. However, the correlation between Veillonella and DMFT/DMFS was not significant (p > 0.05). In Venn diagram analysis, nine genera shared by all samples of two groups, which comprised 71.88% and 67.64% in pSS patients and controls, respectively.DiscussionThese findings indicate a microbial dysbiosis in pSS patients; notably, Veillonella might be recognized as a biomarker in pSS patients. The core microbiome in pSS patients was similar to the systemic healthy population. These provide insight regarding advanced microbial prevention and treatment of severe dental caries in pSS patients. This study also provides basic data regarding microbiology in pSS.

Diets high in animal fats are associated with increased risks of inflammatory bowel disease, but the mechanism remains unclear. In this study, we investigated the effect of high-fat diet (HFD) on the development of experimental colitis in mice. Relative to mice fed low-fat diet (LFD), HFD feeding for 4 wk increased the levels of triglyceride, cholesterol, and free fatty acids in the plasma as well as within the colonic mucosa. In an experimental colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS), mice on 4-wk HFD exhibited more severe colonic inflammation and developed more severe colitis compared with the LFD counterparts. HFD feeding resulted in higher production of mucosal pro-inflammatory cytokines, greater activation of the myosin light chain kinase (MLCK) tight junction regulatory pathway, and greater increases in mucosal barrier permeability in mice following TNBS induction. HFD feeding also induced gp91, an NADPH oxidase subunit, and promoted reactive oxygen species (ROS) production in both colonic epithelial cells and lamina propria cells. In HCT116 cell culture, palmitic acid or palmitic acid and TNF-α combination markedly increased ROS production and induced the MLCK pathway, and these effects were markedly diminished in the presence of a ROS scavenger. Taken together, these data suggest that HFD promotes colitis by aggravating mucosal oxidative stress, which rapidly drives mucosal inflammation and increases intestinal mucosal barrier permeability. NEW & NOTEWORTHY This study demonstrates high-fat diet feeding promotes colitis in a 2,4,6-trinitrobenzenesulfonic acid-induced experimental colitis model in mice. The underlying mechanism is that high-fat diet induces oxidative stress in the colonic mucosa, which increases colonic epithelial barrier permeability and drives colonic mucosal inflammation. These observations provide molecular evidence that diets high in saturated fats are detrimental to patients with inflammatory bowel diseases.

No abstract

No abstract