Does carbon monoxide inhibit proinflammatory cytokine production by fetal membranes?

Aim: Infection-induced inflammation is a common cause of preterm birth. Pharmacologic inhibition of proinflammatory cytokines improves pregnancy outcome in animal models but there are no universally effective therapies for preterm birth in women. Carbon monoxide (CO) has anti-inflammatory properties at low concentrations but its effects on reproductive tissues is unclear.

Effect of oxygen tension on bacteria-stimulated cytokine production by fetal membranes.

Aim: Tissue culture studies indicate that bacterial products stimulate the production of proinflammatory cytokines by reproductive tissues. However, most of these studies have been performed under room air conditions, supplemented with 5% CO₂. In this study, we tested whether O₂ tension affects bacteria-stimulated cytokine production by extra-placental fetal membranes.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) enhances placental inflammation.

Preterm birth is a leading cause of perinatal morbidity and mortality that is often associated with ascending infections from the lower genital tract. Recent studies with animal models have suggested that developmental exposure to the environmental toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can increase the risk of preterm birth in the offspring. How TCDD may modify placental immunity to ascending infections is unclear.

Can carbon monoxide prevent infection-mediated preterm birth in a mouse model?

Problem: Preterm birth is frequently caused by intrauterine infection and inflammation. Recent studies have demonstrated that carbon monoxide (CO), which is produced endogenously, has potent anti-inflammatory properties. Whether or not CO can prevent infection-mediated preterm birth is unknown.