Gastric bacteria as potential biomarkers for the diagnosis of atrophic gastritis.

BACKGROUND: Identification of the risk factors for atrophic gastritis (AG) and prevention of further deterioration of the gastritis are effective approaches to reduce the incidence of gastric cancer. Previous studies found that dysbiosis has been implicated in a wide range of diseases, while the role of gastric bacteria as a biomarker for AG has not been explored. METHODS AND RESULTS: Gastric juices from cases with non-atrophic gastritis (NAG) and AG were collected for investigation of bacterial composition and function. The ß-diversity of microbiota exhibited a significant reduction in AG samples compared with that in NAG samples. Differential abundance analysis revealed that a total of 23 predicted species changed their distributions; meanwhile, all obligate anaerobic bacteria with a relatively high abundance lowered their contents in AG samples. Additionally, the correlation analysis indicated a clear shift in bacterial correlation pattern between the two groups. Functional interrogation of the gastric microbiota showed that bacterial metabolisms associated with enzyme families, digestive system, and endocrine system were downregulated in AG samples. The compositional dissection of "core microbiota" exhibited that oral pathogens, including Porphyromonas gingivalis, Campylobacter gracilis, and Granulicatella elegans, were magnified in AG samples, suggesting that oral diseases may be a trigger factor for early exacerbation of gastritis. Then, the differentially expressed bacteria were used as diagnostic biomarkers for the random forest classifier model for group prediction. CONCLUSIONS: The results showed that bacterial biomarkers could distinguish AG patients from NAG cases with an accuracy of 90% at the genus level.

The toxicity of perfluorodecanoic acid is mainly manifested as a deflected immune function.

BACKGROUND: Perfluorodecanoic acid (PFDA) is a type of perfluoroalkyl acid (PFAA). PFDA has toxicity similar to dioxin; its effect on the body is not through a single target or a single pathway. However, the mechanism at the global level is still unclear. METHODS AND RESULTS: We treated mice with PFDA and characterized the global changes in gene expression in the liver using microarray analyses. The enriched KEGG pathways and GO analyses revealed that PFDA greatly affected the immune response, which was different from the response of gastric cells previously studied. As a proof of principle, the expressions of IL-1ß and IL-18 were both decreased after PFDA treatment, and qRT-PCR and ELISAs verified the reduction of IL-1ß and IL-18 in liver tissues. Mechanistic investigations indicated that PFDA inhibited caspase-1 activation, and decreased the mRNA levels of NLRP1, NLRP3, and NLRC4; thus, suggesting that inflammasome assemblies were suppressed. Further microarray data revealed that cIAP2 and its binding proteins, which are critical for regulating inflammasome assembly, were also repressed by PFDA. In addition, flow cytometry results revealed a significant inhibition of Th1 cell differentiation in the livers of PFDA-treated mice. CONCLUSIONS: The results of this study suggested that one of the main toxic effects of PFDA on livers was the inhibition of immune response.