THE MECHANISMS OF PRETERM LABOR - COMMON GENITAL-TRACT PATHOGENS DO NOT METABOLIZE ARACHIDONIC-ACID TO PROSTAGLANDINS OR TO OTHER EICOSANOIDS

OBJECTIVE: Our aim was to determine the ability of pathogens commonly associated with genital tract infection and preterm labor to incorporate arachidonic acid and to metabolize it to prostaglandins or to other eicosanoids. STUDY DESIGN: Four common genital tract pathogens, Escherichia coli, Streptococcus viridans, Bacteroides fragilis, and a group B beta-hemolytic streptococcus, were incubated with tritium-labeled arachidonic acid for 2 to 48 hours. Uptake of arachidonic acid was calculated from uptake of radioactivity into the organisms. Tritium-labeled arachidonic acid within the medium was separated from any metabolites by high-performance liquid chromatography to assess metabolism of arachidonic acid within the bacteria. RESULTS: Although all organisms were able to take up arachidonic acid, analysis of its metabolism with high-performance liquid chromatography demonstrated that none of these organisms will synthesize cyclooxygenase, lipoxygenase, or epoxygenase products. CONCLUSION: Bacterial infection cannot initiate preterm labor by intrinsic biosynthesis and release of prostaglandins or other eicosanoids by the bacteria themselves.