BackgroundEpidemiological studies in China have revealed that Schistosoma japonicum infection is inversely correlated with metabolic syndrome, even after repeated chemotherapy with praziquantel (PZQ). We investigated the effect of chronic S. japonicum infection, PZQ chemotherapy, and soluble egg antigen (SEA) treatment on whole-body metabolic homeostasis and hepatic insulin sensitivity in mouse models.ResultsInfection with S. japonicum was found to increase whole-body and hepatic insulin sensitivity in mice. PZQ chemotherapy significantly improved the physiological status of infected mice, maintaining Th2 immune-deviation and enhancing hepatic insulin sensitivity. Multiple linear regression analysis revealed positive correlations between anti-inflammatory cytokine expression and insulin signalling-related genes in the liver, as demonstrated by an in vitro stimulated hepatic cell line with IL-13 and IL-22. SEA treatment also improved the glucose tolerance and insulin sensitivity in Lepr db/db mice.ConclusionsThis study indicated that chronic S. japonicum infection with PZQ chemotherapy and SEA treatment can regulate metabolic homeostasis and protect against metabolic syndrome by promoting Th2 and regulatory responses in the liver.Electronic supplementary materialThe online version of this article (10.1186/s13071-017-2400-5) contains supplementary material, which is available to authorized users.

Background: The host-parasite relationship is based on subtle interplay between parasite survival strategies and host defense mechanisms. It is well known that helminth infection, which afflicts more than one billion people globally, correlates with a decreased prevalence of obesity. Dissecting the underlying mechanisms can provide new targets for treating obesity from the host-parasite interaction perspective. Methods: C57BL/6 mice received a normal or high-fat diet (HFD) with or without Sjp40 (one main component of schistosome-derived soluble egg antigens) treatment. Both the loss and gain-of-function experiments by the inhibitor suppression and lentivirus treatment of miR-802 were utilized to elucidate the role of miR-802/AMPK axis in host lipid metabolism. Hepatocyte lipogenesis assay and metabolic parameters were assessed both in vivo and in vitro . The potential interactions among Sjp40, CD36, miR-802, Prkab1, and AMPK were clarified by pull-down, miRNA expression microarray, quantitative RT-PCR, dual-luciferase reporter assay, and western blotting analysis. Results: We showed a link between decreased miR-802 and impaired lipid metabolism in Schistosoma japonicum infected mice. The decreased miR-802 promotes murine Prkab1 or human Prkaa1 expression, respectively, which increases levels of phosphorylated AMPK, resulting in a decrease in hepatic lipogenesis. Also, injection with schistosome-derived soluble egg antigens (SEA) attenuated metabolism. We demonstrated that Sjp40 as a main component of SEA interacted with CD36 on hepatocytes to inhibit miR-802, resulting in the activation of AMPK pathway and subsequent attenuation of lipogenesis. Collectively: Our study reveals the significant role of miR-802/AMPK axis in hepatic lipid metabolism and identifies the therapeutic potential of Sjp40 in treating obesity-related fatty liver.

Background Peroxisome proliferator-activated receptor- (PPAR-) γ plays critical roles in human metabolic disorders and has recently been implicated as a regulator of cellular proliferation and inflammatory responses. Regulatory T cells (Tregs), which express high levels of PPAR-γ protein, have the ability to maintain immune tolerance to self-antigens and regulate immune response to Schistosoma infection. However, mechanisms involved in the resolution of these responses are elusive. Methods Liver and spleen tissue samples in Schistosoma japonicum-infected mice after administration of pioglitazone (a PPAR-γ agonist) were collected. The hepatic and splenic pathologies were detected by H&E and Masson staining. The percentages of Th1/2 and Treg cells in the liver and spleen of each mouse were determined using flow cytometry. Levels of gene expression of PPAR-γ and Foxp3 in tissues or cells were determined using real-time PCR (RT-PCR). Macrophages were treated with pioglitazone in vitro or cocultured with normal purified CD4+ T cells for detecting Treg cells by flow cytometry. The interactions of PPAR-γ with Foxp3 in CD4+ T cells were detected by coimmunoprecipitation. Results Administration of pioglitazone resulted in the prevention of the development of hepatic and splenic pathologies. Activation of PPAR-γ by pioglitazone resulted in increased percentages of CD4+CD25+Foxp3+ Treg cells and decreased percentages of CD3+CD4+IFN-γ+ and CD3+CD4+IL-4+ cells in the liver and spleen of Schistosoma japonicum-infected mice. In addition, the PPAR-γ agonist can induce Treg cells in vitro directly or by modulating the macrophage's function indirectly. Furthermore, through interaction with Foxp3 in CD4+ T cells, the PPAR-γ agonist can promote the expression of Foxp3; however, the inhibitor of PPAR-γ weakened the expression of Foxp3 by modifying the coexpression of Foxp3 and PPAR-γ. Conclusions Our study reveals a previously unrecognized role for PPAR-γ/Foxp3 signaling in regulating the immunopathology that occurs during Schistosoma infection through induction of Treg cells.

PPAR-γ signaling plays a critical role in the regulation of metabolic disorders through promoting regulatory cell response.

As one of the major crops, maize (Zea mays L.) is mainly distributed in tropical and temperate regions. However, with the changes of the environments, chilling stress has become a significantly abiotic stress affecting seed germination and thus the reproductive and biomass accumulation of maize. Herein, we investigated five seed germination-related phenotypes among 300 inbred lines under low-temperature condition (10 °C). By combining 43,943 single nucleotide polymorphisms (SNPs), a total of 15 significant (P < 2.03 ×  10-6) SNPs were identified to correlate with seed germination under cold stress based on the FarmCPU model in GWAS, among which three loci were repeatedly associated with multiple traits. Ten gene models were closely linked to these three variations, among which Zm00001d010454, Zm00001d010458, Zm00001d010459, and Zm00001d050021 were further verified by candidate gene association study and expression pattern analysis. Importantly, these candidate genes were previously reported to involve plant tolerance to chilling stress and other abiotic stress. Our findings contribute to the understanding of the genetic and molecular mechanisms underlying chilling germination in maize.