Perinatal sepsis caused by Williamsia serinedens infection in a 31-year-old pregnant woman.

Williamsia serinedens has been isolated from soil but has not yet been implicated in human disease. We report the first case of perinatal sepsis caused by a dual-morphotype form of Williamsia serinedens in a 31-year-old pregnant woman hospitalized with preterm labor.

Spontaneous preterm birth in African Americans is associated with infection and inflammatory response gene variants.

Objective: The objective of the study was to study the genetic risk factors of spontaneous preterm birth (PTB) in African Americans.

Study Design: Case-control analyses were performed using maternal and fetal deoxyribonucleic acid from 279 African American birth events (82 PTB and 197 term) and 1432 single-nucleotide polymorphisms from 130 candidate genes. Single-locus association and haplotype analyses were performed.

Preterm birth in Caucasians is associated with coagulation and inflammation pathway gene variants.

Spontaneous preterm birth (<37 weeks gestation-PTB) occurs in approximately 12% of pregnancies in the United States, and is the largest contributor to neonatal morbidity and mortality. PTB is a complex disease, potentially induced by several etiologic factors from multiple pathophysiologic pathways. To dissect the genetic risk factors of PTB a large-scale high-throughput candidate gene association study was performed examining 1536 SNP in 130 candidate genes from hypothesized PTB pathways.

Genetic regulation of amniotic fluid TNF-alpha and soluble TNF receptor concentrations affected by race and preterm birth.

Racial disparity in spontaneous preterm birth (PTB) between African Americans and Caucasians in the US is unexplained, but is probably related to differences in amniotic fluid (AF) inflammatory cytokine profiles. Therefore, this study analyzed the association of 34 single nucleotide polymorphisms (SNPs) in TNF-alpha and its receptor genes (TNFR1 and TNFR2) with AF TNF-alpha and soluble TNF receptor (R1 and R2) concentrations in PTB. Samples consisted of African American and Caucasian cases (PTB), and controls (term birth) for which both cytokine, and maternal and fetal genotype data were available.

Patterns of cytokine profiles differ with pregnancy outcome and ethnicity.

Background: Preterm birth (PTB) is hypothesized to be an inflammatory response disease. However, no single factor alone is likely to explain PTB risk. It is more probable that coordinated networks of cytokines affect risk.

Amniotic fluid interleukin-6 increase is an indicator of spontaneous preterm birth in white but not black Americans.

Objective: This study examined the differences in the inflammatory cytokine interleukin (IL)-6 and the immunoinhibitory cytokine IL-10 in the amniotic fluid of black and white women in spontaneous preterm birth.

Methods: In this study, 321 amniotic fluids from cases (preterm birth 36 or fewer weeks' gestation) and controls (normal term delivery longer than 37 weeks' gestation) were collected (147 cases [49 blacks and 98 whites] and 174 controls [85 blacks and 89 whites]) at the time of active labor. IL-6 and IL-10 concentrations were measured by immunoassays.

Human fetal membrane expression of IL-19 and IL-20 and its differential effect on inflammatory cytokine production.

Objective. The objectives of this study were to document the expression of IL-19 and IL-20, localize their expression in human fetal membranes and to examine their influence on the production of other inflammatory cytokines (IL-1, IL-6, IL-8, and TNF-alpha) from placental membranes.Methods.

Differences in the placental membrane cytokine response: a possible explanation for the racial disparity in preterm birth.

Problem: The prematurity rate is higher in African-Americans (AA) compared with Caucasians (C). As spontaneous preterm labor has been hypothesized to be a host inflammatory response disease racial differences in human placental membrane inflammatory cytokine and prostaglandin pathway gene expression patterns between AA and C were examined in this report.

Method Of Study: Placental membranes (amniochorion) collected from AA and C women from cesareans at term were maintained in an organ explant system and stimulated with endotoxin (lipopolysaccharide, LPS).

Racial disparity in membrane response to infectious stimuli: a possible explanation for observed differences in the incidence of prematurity. Community Award Paper.

Objective: This study compares the immune responsiveness of amniochorionic membranes (AC) derived from African American (AA) and white (C) women to an infectious stimulus ex vivo.

Study Design: AC derived from AA and C women were placed in an organ explant culture for 48 hours and then stimulated with endotoxin. Enzyme-linked immunosorbent assay measured the concentration of matrix metalloproteinase 9 (MMP9), tumor necrosis factor-alpha (TNF-alpha), and soluble TNF receptors (sTNFR1 and sTNFR2) in culture media from stimulated and unstimulated AC.

Role of tumor necrosis factor-alpha in the premature rupture of membranes and preterm labor pathways.

Objective: To further delineate the differences between the preterm labor and premature rupture of the membrane pathways, we investigated the role of the inflammatory cytokines as activators of matrix metalloproteinases 2 and 9 in human fetal membranes.

Study Design: Normal amniochorionic membrane that is maintained in an organ explant system was stimulated with interleukin-1beta, tumor necrosis factor-alpha, or interleukin-6. The expression and activity of matrix metalloproteinases 2 and 9 in amniochorion was documented with reverse transcriptase-polymerase chain reaction and specific substrate activity assays.

TNF-alpha promotes caspase activation and apoptosis in human fetal membranes.

Purpose: Increased amniotic fluid tumor necrosis factor (TNF) is a marker of infection when associated with preterm labor and preterm premature rupture of the amniochorionic membranes (PROM). We have noted increased apoptosis in membranes derived from women with PROM. This study examines the role of TNF in promoting fetal membrane apoptosis.