No abstract

Mice immunized with attenuated Salmonella typhimurium, strain SL3235, while protected against virulent challenge, are unable to mount in vivo and in vitro antibody responses to non-Salmonella antigens, such as tetanus toxoid and sheep red blood cells, and exhibit profoundly suppressed responses to B and T cell mitogens. Suppression of antibody responses is mediated by macrophage (M phi)-released soluble factors, and is completely reversed by treatment with interleukin (IL)-4. The present report identifies the suppressor factor as nitric oxide (NO), and provides evidence for a mechanism by which IL-4 abrogates suppression. Suppressed antibody responses correlated with high levels of NO secretion by splenocytes of SL3235-immunized mice. NO production was observed only in cultures consisting of the adherent cell fraction of immune splenocytes. Further, immunosuppression was reversed by NG-monomethyl-L-arginine (NMLA), a competitive inhibitor of NO synthesis, and was completely blocked by the addition of excess L-arginine. Treatment with IL-4, or anti-interferon (IFN)-gamma monoclonal antibody (mAb), also abrogated suppression. Optimal reversal of suppression was observed only when NMLA, IL-4, or anti-IFN-gamma mAb, was added at day 0 of the 5-day plaque-forming cell assay. Treatment with either IL-4 or anti-IFN-gamma mAb also lead to a sharp inhibition of NO production by immune spleen cells. Moreover, the addition of IL-4 to splenic adherent M phi inhibited their ability to generate NO. Our data characterize an immunoregulatory pathway, involving IFN-gamma and NO, by which M phi mediate immunosuppression and identify IL-4 as a potent inhibitor of this pathway.

No abstract

No abstract

No abstract

No abstract

The study aimed to reveal the risk factors and predict the prevalence of human cystic echinococcosis (CE) in Western China. To do this, we analyzed county-wide data relating to the prevalence of human CE in seven provinces of Western China, along with associated human, natural geographical environmental data. We then used spatial analysis and multiple regression analysis to investigate the correlation between the prevalence of human CE and associated environmental factors and to create a risk map of the disease in the seven provinces. Our analysis showed that grassland area ratio and Tibetan population ratio were independent variables positively correlated with the prevalence of human CE and that gross domestic product (GDP) and land surface temperature (LST; Spring) were negative independent variables. We also created a predictive risk map of human CE that revealed that the high-risk areas were mainly located in the south of Qinghai, the Northwest of Sichuan and most of the Tibet Autonomous Region. Knowledge of the spatial distribution and risk factors associated with human CE could help to prevent and control echinococcosis in China.

No abstract