Intervention with fructooligosaccharides, Saccharomyces boulardii, and their combination in a colitis mouse model.

Objective: To examine the effects of an intervention with fructooligosaccharides (FOS), Saccharomyces boulardii, and their combination in a mouse model of colitis and to explore the mechanisms underlying these effects. Methods: The effects of FOS, S. boulardii, and their combination were evaluated in a DSS-induced mouse model of colitis. To this end, parameters such as body weight, the disease activity index (DAI), and colon length were examined in model mice. Subsequently, ELISA was employed to detect the serum levels of proinflammatory cytokines. Histopathological analysis was performed to estimate the progression of inflammation in the colon. Gas chromatography was used to determine the content of short-chain fatty acids (SCFAs) in the feces of model mice. Finally, 16S rRNA sequencing technology was used to analyze the gut microbiota composition. Results: FOS was slight effective in treating colitis and colitis-induced intestinal dysbiosis in mice. Meanwhile, S. boulardii could significantly reduced the DAI, inhibited the production of IL-1ß, and prevented colon shortening. Nevertheless, S. boulardii treatment alone failed to effectively regulate the gut microbiota. In contrast, the combined administration of FOS/S. boulardii resulted in better anti-inflammatory effects and enabled microbiota regulation. The FOS/S. boulardii combination (109 CFU/ml and 107 CFU/ml) significantly reduced the DAI, inhibited colitis, lowered IL-1ß and TNF-α production, and significantly improved the levels of butyric acid and isobutyric acid. However, FOS/S. boulardii 109 CFU/ml exerted stronger anti-inflammatory effects, inhibited IL-6 production and attenuated colon shortening. Meanwhile, FOS/S. boulardii 107 CFU/ml improved microbial regulation and alleviated the colitis-induced decrease in microbial diversity. The combination of FOS and S. boulardii significantly increased the abundance of Parabacteroides and decreased the abundance of Escherichia-Shigella. Additionally, it promoted the production of acetic acid and propionic acid. Conclusion: Compared with single administration, the combination can significantly increase the abundance of beneficial bacteria such as lactobacilli and Bifidobacteria and effectively regulate the gut microbiota composition. These results provide a scientific rationale for the prevention and treatment of colitis using a FOS/S. boulardii combination. They also offer a theoretical basis for the development of nutraceutical preparations containing FOS and S. boulardii.

Serum Metabonomics of Articular Cartilage Destruction Induced by T-2 Toxin in Wistar Rats.

The molecular pathogenesis of T-2 toxin-induced cartilage destruction has not been fully unraveled yet. The aim of this study was to detect changes in serum metabolites in a rat anomaly model with articular cartilage destruction. Thirty healthy male Wistar rats were fed a diet containing T-2 toxin (300 ng/kg chow) for 3 months. Histopathological changes in femorotibial cartilage were characterized in terms of chondrocyte degeneration/necrosis and superficial cartilage defect, and the endogenous metabolite profile of serum was determined by UPLC/Q-TOF MS. Treated rats showed extensive areas of chondrocyte necrosis and superficial cartilage defect in the articular cartilage. In addition, 8 metabolites were found to change significantly in these rats compared to the control group, including lysoPE (18:0/0:0), lysoPC(14:0), lysoPC[18:4 (6Z,9Z,12Z,15Z)], lysoPC[(16:1(9Z)], lysoPC(16:0), L-valine, hippuric acid, and asparaginyl-glycine. These 8 metabolites associated with cartilage injury are mainly involved in phospholipid and amino acid metabolic pathways.

Retrospective study of risk factors for mortality in human avian influenza A(H7N9) cases in Zhejiang Province, China, March 2013 to June 2014.

BACKGROUND: The influenza A(H7N9) virus causes a serious disease that threatens human health. Fatalities associated with human infections caused by this virus are of great public health concern; however, the possible risk factors are not yet fully known. METHODS: A stratified sampling method, incorporating household income levels and a random number table method, was used to select laboratory-confirmed A(H7N9) cases for this study. Eighty-five patients were selected randomly from 139 laboratory-confirmed A(H7N9) cases occurring in Zhejiang Province between March 1, 2013 and June 30, 2014. Data were collected using a standard method. To test the statistical significance among discrete variables, univariate analyses were used to compare two groups. The Kaplan-Meier product-limit method was used to analyze the patient survival fraction. The Cox proportional hazards regression model was used to analyze all variables with p ≤ 0.05 in the univariate analysis. Lastly, a stepwise procedure was used to construct a final model with a significance level of p > 0.10 for removal and p<0.05 for re-entry. RESULTS: A total of 85 patients with H7N9 virus infection were identified. Among these, 30 (35.29%) died. In the univariate analysis, the following factors were associated with a high risk of influenza A(H7N9) case fatality: age ≥ 60 years (p=0.008), low education level (p=0.030), chronic diseases (p=0.029), poor hand hygiene (p=0.010), time from illness onset to the first medical visit (p=0.029) and to intensive care unit admission (p=0.008), an incubation period of ≤ 5 days (p=0.039), a peak C-reactive protein ≥ 120 mg/l (p=0.012), increased initial neutrophil count (p=0.020), decreased initial lymphocyte count (p=0.021), and initial infection of both lungs (p=0.003). Multivariate analysis confirmed that the independent predictors of H7N9 virus infection mortality in Zhejiang, China were hand hygiene (hazard ratio (HR) 5.163, 95% confidence interval (CI) 1.164-22.661), age (HR 1.042, 95% CI 1.007-1.076), and peak CRP (HR 1.009, 95% CI 1.002-1.016). CONCLUSIONS: Improvements in immunity, early case identification and treatment, and personal protection measures are key to addressing the high human avian influenza A(H7N9) case fatality rate.

Epidemiologic characterization of 30 confirmed cases of human infection with avian influenza A(H7N9) virus in Hangzhou, China.

BACKGROUND: We examined the clinical and epidemiological characteristics of 30 cases of human infection with avian influenza A(H7N9) virus in Hangzhou and investigated their external environments to provide evidence for contact tracing and disease prevention and control. METHODS: The cases confirmed from April 1 through May 1, 2013 were studied. Field epidemiologic surveys were conducted to collect the clinical and epidemiologic data. Case-related and environmental specimens were collected for etiologic detection. RESULTS: Thirty cases of human infection with avian influenza A(H7N9) virus were confirmed in Hangzhou from April 1 through May 1, 2013, including one pregnant woman and three deaths. The median age of the patients was 62 years (range: 38-86 years). Twenty-three of the patients were men (76.67%). The median duration between disease onset and occurrence of respiratory failure and confirmed diagnosis was 5 and 6 days, respectively. Maximum medical observation of 666 close contacts of the patients revealed no irregularity. Of 314 external environmental specimens, the overall positive detection rate of H7N9 nucleic acid was 28.98%. Eight districts of Hangzhou city had positive detections in the external environments, the highest rate being in Yuhang District (78.13%). Statistical analysis of the specimen collection locations indicates a significant difference between the case-linked locations and the non-case locations (χ2 = 16.563, p < 0.05) in terms of H7N9 viral nucleic acid detection rate. No epidemiologic link has been found among the 30 cases. CONCLUSIONS: Most of the infected were retired individuals aged 60 years or older. Men made the majority. The cases are sporadic at present, with no evidence of human-to-human transmission. Exposures to poultry and live poultry markets may be important sources of infection.