Magnesium sulfate does not have a major impact on disease progression in women with mild preeclampsia. Magnesium use does not seem to increase rates of cesarean delivery, infectious morbidity, obstetric hemorrhage, or neonatal depression.
Attempts at asynchronous deliveries are uncommon and are associated with a high rate of perinatal death. Most fetal survivors have significant damage from preterm birth.
Ureaplasma urealyticum and Mycoplasma hominis, two genital mycoplasmas, are the most common organisms isolated in the perinatal period and both either cause or are associated with poor perinatal outcomes. We speculate that these microbes could increase inflammation by stimulating macrophages to produce tumor necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase because of their propensity to interact with the host's immune system. To test this hypothesis, RAW 264.7 cells, a murine macrophage cell line, were coincubated for 16 h with either U. urealyticum or M. hominis, and LPS and sterile broth were used as controls. Lipopolysaccharide (LPS) and both mycoplasmas induced TNF-alpha production, which was concentration-dependent, whereas sterile broth had little effect. TNF-alpha production was not inhibited by the addition of polymyxin B, excluding the possibility of contaminating endotoxin in this effect. Inducible nitric oxide synthase was produced only in the presence of recombinant inteferon-gamma. We conclude that both viable and nonviable U. urealyticum and M. hominis are capable of TNF-alpha induction from murine macrophages and that LPS is not involved in this event. Also, the genital mycoplasmas are capable of stimulating inducible nitric oxide synthase production from murine macrophages. We speculate that the genital mycoplasmas produce perinatal disease by producing proinflammatory mediators by their interaction with inflammatory cells and either induce or act as a catalyst and augment inflammation which in turn leads to a poor pregnancy outcome.
Tumor necrosis factor-a (TNF-a) is a proinflammatory cytokine that appears to play a significant role in the development of neonatal chronic lung disease (CLD). Inflammation and CLD are also associated with respiratory tract colonization with genital mycoplasmas. The possible protective roles of surfactant in mitigating the inflammatory response to these microbes were investigated. Murine RAW 264.7 macrophages were preincubated with an exogenous surfactant and exposed overnight to sterile media, lipopolysaccharide (LPS), Mycoplasma hominis, or Ureaplasma urealyticum. Macrophages released TNF-a in response to challenge with LPS, U. urealyticum, and M. hominis in a concentration-dependent fashion. Surfactant suppressed LPS and M. hominis induced TNF-a production in a dose-dependent manner but suppressed U. urealyticum -mediated TNF-a production only at the higher dose tested. Similar effects were seen in hyperoxia (95% O 2 ). Thus, exogenous bovine surfactant significantly inhibits the production of TNF-a by murine macrophages stimulated with genital mycoplasmas and bacterial LPS.
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