Background: Type 2 diabetes (T2DM) is a top risk factor for health in China. Gut microbiota, genetic factors and lipids metabolism play important role in development of T2DM. In this study, we investigated the relationship between the gut microbiota and omentin-1 gene polymorphism to explore the interaction between host gene and gut microbiota in Uyghur T2DM. Methods: A total of 98 newly diagnosed Uyghur T2DM patients and 99 healthy normal controls (NC) enrolled into this study according to inclusion criteria. The total DNAs was extracted from the fecal microbiota. Abundance of the Lactobacillus genus, Bacteroides thetaiotaomicron and Clostridium in the gut microbiota was determined with 16S rDNA gene Real-time fluorescence quantitative PCR amplification. PCR-PFLP was applied to determine the genotypes of Val109Asp variant (rs2274907) in the Omentin-1 gene. And the relationship between rs2274907 and gut microbiota was assessed. Results: There were no significant differences of the Val109Asp variant (rs2274907) between T2DM and NC group. The abundance of Lactobacillus genus and Clostridium genus was lower in newly diagnosed T2DM group than in the NC group (P<0.05). Serum insulin, LDL-C, the abundances of Lactobacillus genus and Clostridium genus were the risk factors of T2DM. (OR=1.094 95%CI 1.014-1.180), (OR=3.868 95%CI 1.250-11.971), (OR=0.288 95%CI 0.145-0.571), (OR=0.044 95%CI 0.012-0.154). Conclusions: The abundance of Lactobacillus and Clostridium genus may be related to the pathogenesis of new-onset T2DM in Uyghur population, the mechanism of which needs to be further studied. The interactive relationship between the gut microbiota and omentin-1 gene polymorphism in newly diagnosed T2DM was not observed in this study.

Background Alveolar echinococcosis (AE) is a potentially lethal zoonosis caused by the cestode Echinococcus multilocularis. The aim of this study is to study the dynamic changes of monocytes, macrophages and related cytokines in animal models of persistent infection of Echinococcus multilocularis. To explore the possible connection between them and the persistent infection of Echinococcus multilocularis.Methods An infection model was established by intraperitoneal injection of a protoscolex suspension. The pathological changes of mice liver were observed by HE staining and the score scale of infection was established. The ratio of Ly6Chi and Ly6Clo Monocytes in peripheral blood of mice was detected by flow cytometry. The distribution and expression of CX3CL1, CX3CR1, iNOS, CD163 and CD11b in mouse liver were detected by immunohistochemistry. The mRNA expression levels of TNF-α and Arg1 in mouse liver were detected by qRT-PCR. The expression levels of INF-γ, IL-17, IL-4 and IL-10 in peripheral blood of mice were detected by ELISA.Results The results of HE staining showed that in the later stages of infection, significant lesions appear in the liver.The results of the infection degree score scale show that with the extension of the infection time, the severity score value increases. The results of flow cytometry showed that the proportion of Ly6Chi monocytes in the peripheral blood of the experimental group mice was decreased after a brief rise, Ly6Clo monocytes decreased first and then increased.. The results of immunohistochemistry showed that the expression of CX3CL1, CX3CR1, CD11b , CD163 and iNOS in the mice liver of the experimental group was increased. The results of qRT-PCR showed that the expression level of TNF-α and Arg1 mRNA in the liver of the experimental group mice were increased. The results of ELISA showed that the expression level of IFN-γ, IL-17, IL-4 and IL-10 increased with the duration of infection.Conclusions Monocytes as a supplement to hepatic macrophage, it and kupffer cells (KCs) participate in Th1 and Th2 immune responses of the body by differentiating into M1 or M2 at different stages of Echinococcus multilocularis infection.

Background: The cestode Echinococcus multilocularis (E. multilocularis) infection, a serious health problem worldwide, causes alveolar echinococcosis (AE), a tumor-like disease predominantly located in the liver and able to spread to any organs. Until now, there have been few studies that explain how TIM-1+B cells contribute to the immune tolerance in E. multilocularis infection.Methods: Hematoxylin-eosin (H&E) and Masson staining were used to assess the pathological inflammatory changes and collagen deposition respectively in the liver of E. multilocularis infected mice. Desmin, TIM-1 and IL-10 were detected by immunohistochemistry (IHC). qRT-PCR and ELISA were used to detect the IL-10 of liver and serum, respectively. Flow cytometry was used to assess the level and function of CD19+TIM-1+ cells and CD19+CD5+CD1dhi cells in spleen. Immunofluorescence (IF) were used to detect the co-localization of immune cells in the liver.Results: At 180 days after infection, inflammatory cells and fibrosis could be observed in the liver of mice in the infection group, a large number of activated hepatic stellate cells (HSC) and TIM-1+ cells appeared around the lesion and the expression of IL-10 was also significantly higher than that in control group. The level and function of CD19+TIM-1+ cells and CD19+CD5+CD1dhi cells in the spleen were up-regulated in the infection group, but CD19+TIM-1+ cells produced IL-10 more efficiently and could be recruited to the lesion.Conclusions: In the late stage of alveolar echinococcosis, CD19+TIM-1+ cells can be recruited to the lesion and may be more efficient IL-10 producers to participate in the formation of immune tolerance.