Interleukin-12p70 / IL-12p70 (Mouse) ELISA KIT

Interactions between genetic variation and environmental factors have been invoked in schizophrenia genesis, but pathways linking them are uncertain. We used a pathway-oriented approach to evaluate six genes mediating IL18 function (IL-18, IL18BP, IL18R1, IL18RAP, IL12B, and IL12A). The first five are also localized to regions previously linked with schizophrenia. Fifty-four representative tag SNPs were selected from comprehensive sequence data and genotyped in 478 patients with schizophrenia/schizoaffective disorder (DSM IV criteria) and 501 unscreened control individuals. Exposure to three herpes viruses previously suggested as risk factors for schizophrenia was estimated simultaneously among the cases. Five SNPs in four genes were associated with schizophrenia, most prominently rs2272127 at IL18RAP (P = 0.0007, odds ratio for C allele 1.49, 95% CI: 1.18-1.87; P = 0.03 following correction for multiple comparisons). Exploratory analysis revealed that rs2272127 was also associated with herpes simplex virus 1 (HSV1) seropositivity in cases (P = 0.04, OR for G allele 1.58, 95% CI: 1.04-2.39). Similar patterns were observed at another correlated SNP (rs11465702, P = 0.005 and 0.006, respectively for associations with schizophrenia and HSV1 seropositivity). We suggest plausible, testable hypotheses linking IL-18 signaling and HSV1 in schizophrenia pathogenesis. (C) 2007 Wiley-Liss, Inc.

Fascioliasis is a disease caused by liver flukes. In human fascioliasis hyperendemic areas, reinfection and chronicity are the norm. Control strategies in humans require the use of egg count techniques to calculate the appropriate treatment dose for colic risk prevention. The present study investigates how fascioliasis reinfection affects liver fluke egg shedding and its relationship with the immune-regulatory response. The experimental design reproduced the usual reinfection/chronicity conditions in human fascioliasis endemic areas and included Fasciola hepatica primo-infected Wistar rats (PI) and rats reinfected at 4 weeks (R4), 8 weeks (R8), 12 weeks (R12), and negative control rats. In a longitudinal study (0-20 weeks post-infection, p.i.), serical IgG1 levels and eggs per gram of faeces (epg) were analyzed. In a cross-sectional study, the expression of the genes associated with Th1 (Ifng, Il12a, Il12b, Nos2), Th2 (Il4, Arg1), Treg (Foxp3, Il10, Tgfb, Ebi3), and Th17 (Il17) in the spleen and thymus was analyzed. In R8 and R12, transiently higher averages of epg and epg/worm in reinfected groups vs PI group were detected at least in the weeks following reinfection. The kinetics of IgG1 levels shows that reinfected groups followed a pattern similar to the one in the PI group, but transiently higher averages of IgG1 levels in reinfected groups vs the PI group were detected in the weeks following reinfection. Epg correlated with IgG1 levels and also with systemic Il10 and thymic Ifng, and Il10 expression levels. These results suggest that epg depends on the Th1 and Treg phenotype and that the determination of the fluke burden by epg is likely to be an overestimation in cases of recent reinfection in low burden situations. A strategy to facilitate the implementation of epg count techniques and the subsequent decision on the appropriate treatment dose for each patient to prevent colic risk is required.