Schistosomes infect ϳ40 million women of childbearing age and result in the elaboration of proinflammatory cytokines that have been implicated in fetal growth restriction. In murine models and two observational studies in humans, schistosome infection during pregnancy was associated with reduced birth weight, although a recent treatment trial in Schistosoma mansoni did not detect this association. We conducted an observational study among 99 pregnant women living in an area of Schistosoma japonicum endemicity in the Philippines. We enrolled women at 32 weeks gestation and measured S. japonicum and geohelminth infection intensity. We collected maternal peripheral blood at 32 weeks gestation and placental and cord blood at delivery to assess inflammatory status. At delivery, we collected a placental-tissue sample and measured birth weight. In multivariate models adjusted for geohelminths, maternal schistosomiasis was associated with increased levels of inflammatory cytokines in maternal peripheral (tumor necrosis factor alpha [TNF-␣] and interleukin 10 [IL-10]), placental (TNF-␣, IL-6, TNF-␣ receptor II [RII], and IL-1), and cord (IL-1 and TNF-␣ RII) blood, as well as acute subchorionitis and increased TNF-␣ production by syncytiotrophoblasts assessed by immunohistochemistry (all P < 0.05). After adjusting for confounders, placental IL-1, and TNF-␣ production by syncytiotrophoblasts was independently associated with decreased birth weight (both P < 0.05). Our data indicate that maternal schistosomiasis results in a proinflammatory signature that is detectable in maternal, placental, and fetal compartments, and a subset of these responses are associated with decreased birth weight. This potential mechanistic link between maternal schistosomiasis and poor birth outcomes will contribute to the debate regarding treatment of maternal schistosome infections.Healthy successful pregnancies are characterized by a placental microenvironment that is biased toward a T-helper cell type 2 (Th2) cytokine milieu (16,23). Parasitic diseases, including malaria and leishmaniasis, alter the placental Th2 bias toward a proinflammatory microenvironment and are associated with poor pregnancy outcomes (29,39,48). These data are consistent with animal models of pregnancy that establish that increased systemic and placental gamma interferon (IFN-␥) and tumor necrosis factor alpha (TNF-␣) levels produce poor pregnancy outcomes (10, 50). They are also consistent with the marked increase in prematurity and IUGR accompanying human pregnancies complicated by systemic proinflammatory diseases, such as systemic lupus erythematosis, rheumatoid arthritis, and falciparum malaria (18,33,55).Human schistosomiasis, caused by three main species of tissue-invasive parasitic trematodes, infects over 200 million individuals, including ϳ40 million women of childbearing age, and remains a significant cause of morbidity and mortality in developing countries (35). Human infection with schistosomes results in the elaboration of proinflammatory cytokines, inc...
Although animal models have been used successfully to study metabolic activation and binding of carcinogens to DNA, only limited studies have been done in human systems. To circumvent the problems associated with the inaccessibility of human tissues and a lack of sensitive methods to detect DNA damage, we have investigated the capability of human peripheral blood lymphocytes in vitro to metabolize carcinogens to their DNA binding species by a 32P-labeled adduct assay. Freshly isolated lymphocytes were exposed at 37TC for 18 hr to 4-aminobiphenyl, 2
In an attempt to understand the relationship between the CD23 antigen and the human 12-kDa B cell growth factor (BCGF) receptor, we have undertaken studies to define the biological efficacy of 12-kDa-BCGF on CD23+ (Raji) and CD23- (P3HR1) human Burkitt B cell lines. Our results show that recombinant 12-kDa-BCGF can induce efficient [3H]thymidine incorporation and proliferation in cells of either phenotype. These results strongly suggest that a functional receptor for the 12-kDa-BCGF may exist independently of the CD23 molecule.
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