Alison P Sanders1, Chris Gennings1, Katherine Svensson1, Valeria Motta2,3, Adriana Mercado-Garcia4, Maritsa Solano4, Andrea A Baccarelli2,5, Martha M Tellez-Rojo4, Robert O Wright1, Heather H Burris5,6,7. 1. Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, NY 10029, USA. 2. Laboratory of Environmental Epigenetics, Exposure Epidemiology & Risk Program, Harvard TH Chan School of Public Health, Boston, MA 02115, USA. 3. Department of Clinical Sciences & Community Health University of Milan - Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan 20122, Italy. 4. Center for Evaluation Research & Surveys, National Institute of Public Health, Cuernavaca, Morelos 62100, Mexico. 5. Department of Environmental Health, Harvard TH Chan School of Public Health, Boston, MA 02115, USA. 6. Boston Children's Hospital & Harvard Medical School, Boston, MA, USA. 7. Division of Newborn Medicine, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Abstract
AIM: Bacterial vaginosis may lead to preterm birth through epigenetic programming of the inflammatory response, specifically via miRNA expression. METHODS: We quantified bacterial 16S rRNA, cytokine mRNA and 800 miRNA from cervical swabs obtained from 80 women at 16-19 weeks' gestation. We generated bacterial and cytokine indices using weighted quantile sum regression and examined associations with miRNA and gestational age at delivery. RESULTS & DISCUSSION: Each decile of the bacterial and cytokine indices was associated with shorter gestations (p < 0.005). The bacterial index was associated with miR-494, 371a, 4286, 185, 320e, 888 and 23a (p < 0.05). miR-494 remained significant after false discovery rate correction (q < 0.1). The cytokine index was associated with 27 miRNAs (p < 0.05; q < 0.01). CONCLUSION: Future investigation into the role of bacterial vaginosis- and inflammation-associated miRNA and preterm birth is warranted.
AIM: Bacterial vaginosis may lead to preterm birth through epigenetic programming of the inflammatory response, specifically via miRNA expression. METHODS: We quantified bacterial 16S rRNA, cytokine mRNA and 800 miRNA from cervical swabs obtained from 80 women at 16-19 weeks' gestation. We generated bacterial and cytokine indices using weighted quantile sum regression and examined associations with miRNA and gestational age at delivery. RESULTS & DISCUSSION: Each decile of the bacterial and cytokine indices was associated with shorter gestations (p < 0.005). The bacterial index was associated with miR-494, 371a, 4286, 185, 320e, 888 and 23a (p < 0.05). miR-494 remained significant after false discovery rate correction (q < 0.1). The cytokine index was associated with 27 miRNAs (p < 0.05; q < 0.01). CONCLUSION: Future investigation into the role of bacterial vaginosis- and inflammation-associated miRNA and preterm birth is warranted.
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