4.6 Article

Clinical chorioamnionitis at term: the amniotic fluid fatty acyl lipidome

Journal

JOURNAL OF LIPID RESEARCH
Volume 57, Issue 10, Pages 1906-1916

Publisher

ELSEVIER
DOI: 10.1194/jlr.P069096

Keywords

lipoxygenase; eicosanoids; inflammation; omega-3 fatty acids; lipidomics; intra-amniotic inflammation; infection; parturition; epoxy fatty acids; epoxygenase

Funding

  1. Perinatology Research Branch, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Department of Health and Human Services
  2. NICHD (Foundation for the National Institutes of Health) [HHSN275201300006C]
  3. National Center for Research Resources (Foundation for the National Institutes of Health) [S10RR027926]
  4. Perinatal Virtual Discovery Grant from Wayne State University

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Clinical chorioamnionitis at term (TCC) is the most common obstetrical infliction diagnosed in labor and delivery units worldwide and is associated with a substantial increase in maternal and neonatal morbidity and mortality. This obstetrical complication is a heterogeneous condition, as only half of patients have detectable microorganisms in the amniotic cavity. Because bioactive lipids play a key role in the initiation and resolution of an inflammatory response, we aimed to characterize the amniotic fluid lipidome in patients with TCC. We studied the amniotic fluid of patients in the following groups: 1) spontaneous labor at term without clinical chorioamnionitis (TLB) and 2) spontaneous labor at term with clinical chorioamnionitis (TCC). The TCC group was subdivided into a) those with microbial invasion of the amniotic cavity (TCC-MIAC) and b) those without microbial invasion of the amniotic cavity (TCC-noMIAC). The amniotic fluid concentration of proinflammatory lipid mediators did not differ between patients in TLB with TCC. In contrast, concentration of lipids with anti-inflammatory/proresolution properties was significantly lower in all patients with TCC than in those with TLB. These results suggest that while proinflammatory lipid mediators are involved in infection-driven intra-amniotic inflammation, a relative deficiency of anti-inflammatory/proresolution lipid mediator biosynthesis is a characteristic of TCC.

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