Morgan Peltier

Effect of Progesterone on Proinflammatory Cytokine Production by Monocytes Stimulated with Pathogens Associated with Preterm Birth

Problem A number of clinical trials have demonstrated that supplemental progesterone (P4) can prevent preterm birth. Although P4 can decrease the production of mediators of inflammation by lipopolysaccharide (LPS)‐stimulated macrophages, a majority of infections associated with preterm birth are due to Ureaplasma urealyticum, which does not contain LPS. Therefore, we studied whether P4 could lower the production of proinflammatory cytokines by monocytes stimulated with U. urealyticum.

Can sulfasalazine prevent infection-mediated pre-term birth in a murine model?

Citation Nath CA, Ananth CV, Smulian JC, Peltier MR. Can sulfasalazine prevent infection‐mediated pre‐term birth in a murine model? Am J Reprod Immunol 2010; 63: 144–149

Characterization and Partial Purification of a Macrophage-Stimulating Factor from Mycoplasma hominis

Mycoplasma hominis is one of the most common pathogens of the genital tract and is associated with increased production of proinflammatory cytokines in reproductive tissues during preterm labor. The mechanism by which M. hominis, an organism lacking cell walls, increases the production of proinflammatory cytokines is unknown.

Experimental Genital Mycoplasmosis Causes Increased Levels of mRNA for IL‐6 and TNF‐α in the Placenta

Problem:u2002 Previous studies with animal models have shown that injection of lipopolysaccharide (LPS) results in fetal loss and increases production of proinflammatory cytokines at the maternal–fetal interface. Most intrauterine infections, however, are associated with Ureaplasma urealyticum, a microorganism that lacks a cell wall and therefore does not contain LPS. Previous work in our laboratory with an animal model for genital infection with a similar organism, Mycoplasma pulmonis, revealed that widespread infection in maternal and fetal tissues can be experimentally induced with minimal manipulation of the animal. For this project, we tested the hypothesis that administration of the organism by a hematogenous route at gestational day (gd) 14 would result in increased tumor necrosis factor (TNF)‐α and interleukin (IL)‐6 production by the placenta.

Thromboembolic diseases in families of women with placental abruption.

Background: We explored the incidence of thromboembolic disease in relatives of women diagnosed with placental abruption, a condition that may be related to disordered coagulation. Methods: Using data from a multicenter, case-control study of placental abruption, we assessed thromboembolic diseases in first-degree male and female relatives of women with and without abruption. The analysis was restricted to biologic parents and full siblings, below 65 years of age, and corrected for familial clustering. Results: The prevalence of thromboembolic disease was 7.5% in 852 relatives of 212 placental abruption cases and 4.8% in 792 relatives of 206 controls. This increased risk was driven by an association among sisters of abruption probands (odds ratio = 6.8 [95% confidence interval = 1.8–26.0]), and to a lesser extent, among mothers (2.0 [1.0–4.2]). The risk of thromboembolic diseases was similar among the male relatives of placental abruption cases and controls. Conclusions: These data suggest that thromboembolic diseases aggregate within female relatives of women with placental abruption.

Effect of sulfasalazine on basal and bacteria-stimulated interleukin-8 production by endocervical epithelial cells.

Problemu2002 Sulfasalazine (SASP) inhibits lipopolysaccharide‐induced nuclear‐factor kappa B activation and interleukin‐8 (IL‐8) production by cultured explants of placenta, amnion and choriodecidua. Bacteria‐induced IL‐8 production in the cervix is a potential mechanism for premature cervical ripening that may lead to preterm birth. Our objective was to determine if SASP inhibits IL‐8 production by endocervical cells stimulated with bacterial pathogens associated with preterm birth.