American Journal of Obstetrics & Gynecology
Volume 200, Issue 3 , Pages 334.e1-334.e8, March 2009

Distinct pathophysiologic pathways induced by in vitro infection and cigarette smoke in normal human fetal membranes

Presented at the 75th Annual Meeting of the Central Association of Obstetricians and Gynecologists, New Orleans, LA, Oct. 22-25, 2008.

  • Ramkumar Menon, PhD

      Affiliations

    • Perinatal Research Center, Nashville, TN
    • Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA
    • Corresponding Author InformationReprints: Ramkumar Menon, PhD, The Perinatal Research Center, Centennial Women's Hospital, 2300 Patterson St, Nashville, TN 37203
    • ,
  • Stephen J. Fortunato, MD

      Affiliations

    • Perinatal Research Center, Nashville, TN

Received 1 July 2008; received in revised form 28 December 2008; accepted 29 December 2008.

Objective

The purpose of this study was to document distinct pathways that are initiated by lipopolysaccharide and cigarette smoke stimulation of normal term fetal membranes.

Study Design

Fetal membranes from nonsmoking women at term, not in labor, from cesarean deliveries were placed in an organ explant system and stimulated with cigarette smoke extracts (CSEs), lipopolysaccharide, or lipopolysaccharide + CSE. Media were assayed for an interleukin (IL)-1β, -1 receptor antagonist, -6, -8, -10, tumor necrosis factor α, soluble tumor necrosis factor receptors 1 and 2, and matrix metalloproteinases 1, 2, 3, 8, 9, and 12. Tissue homogenates were assayed for apoptotic markers (p53, caspase 3 activity, and cleaved poly [ADP-ribose] polymerase-1).

Results

Lipopolysaccharide stimulation resulted in higher cytokine and matrix metalloproteinase concentrations, whereas it was lower after CSE and CSE + lipopolysaccharide stimulations, compared with control specimens. Apoptotic factors were several folds higher after CSE or CSE + lipopolysaccharide stimulation, compared with control specimens or lipopolysaccharide stimulations.

Conclusion

Cigarette smoke showed immunoinhibitory properties that potentially were mediated by apoptosis and lipopolysaccharide-induced proinflammatory response. This study demonstrated 2 independent pathophysiologic pathways that may alter pregnancy outcome.

Key words: behavioral factor, cigarette smoke, cytokine, fetal membrane, pPROM, toxin

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 Cite this article as: Menon R, Fortunato SJ. Distinct pathophysiologic pathways induced by in vitro infection and cigarette smoke in normal human fetal membranes. Am J Obstet Gynecol 2009;200:334.e1-334.e8.

 Authorship and contribution to the manuscript is limited to the 2 authors indicated. There was no outside funding or technical assistance with the production of this article.

PII: S0002-9378(08)02459-9

doi:10.1016/j.ajog.2008.12.051

American Journal of Obstetrics & Gynecology
Volume 200, Issue 3 , Pages 334.e1-334.e8, March 2009

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