Nardhy Gomez-Lopez1,2,3, Roberto Romero1,4,5,6, Marcia Arenas-Hernandez1,2, Bogdan Panaitescu1,2, Valeria Garcia-Flores1,2, Tara N Mial1,2, Aashna Sahi2, Sonia S Hassan1,2. 1. a Perinatology Research Branch, Program for Perinatal Research and Obstetrics, Division of Intramural Research , Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, U.S. Department of Health and Human Services , Bethesda , MD , and Detroit , MI , USA. 2. b Department of Obstetrics and Gynecology , Wayne State University School of Medicine , Detroit , MI , USA. 3. c Department of Immunology and Microbiology , Wayne State University School of Medicine , Detroit , MI , USA. 4. d Department of Obstetrics and Gynecology , University of Michigan , Ann Arbor , MI , USA. 5. e Department of Epidemiology and Biostatistics , Michigan State University , East Lansing , MI , USA. 6. f Center for Molecular Medicine and Genetics , Wayne State University , Detroit , MI , USA.
Abstract
OBJECTIVE: Intra-amniotic infection is associated with spontaneous preterm labor. In most cases, the infection is subclinical and bacteria are detected in the amniotic cavity rather than in the chorioamniotic membranes. The aims of this study were to establish a model of intra-amniotic lipopolysaccharide (LPS)-induced preterm labor/birth that resembles the subclinical syndrome and to compare this model to two established models of LPS-induced preterm labor/birth. METHODS: Pregnant B6 mice received an intra-amniotic, intra-uterine, or intra-peritoneal injection of LPS (100 ng/amniotic sac, 15 μg/25 μL, and 15 μg/200 μL respectively) or PBS (control). Following injection, body temperature (every two hours for a 12-h period), gestational age, and the rate of preterm labor/birth were recorded. RESULTS: An intra-amniotic injection of LPS resulted in preterm labor/birth [LPS 80 ± 24.79% (8/10) versus PBS 0% (0/8); p = 0.001] without causing maternal hypothermia. Intra-peritoneal [LPS 100% (8/8) versus PBS 0% (0/8); p < 0.001)] and intra-uterine [LPS 100% (8/8) versus PBS 28.57 ± 33.47% (2/7); p =0 .007] injections of LPS induced preterm labor/birth; yet, maternal hypothermia was observed. CONCLUSION: Intra-amniotic injection of LPS induces preterm labor/birth in the absence of a body temperature change, which resembles the subclinical syndrome.
OBJECTIVE:Intra-amniotic infection is associated with spontaneous preterm labor. In most cases, the infection is subclinical and bacteria are detected in the amniotic cavity rather than in the chorioamniotic membranes. The aims of this study were to establish a model of intra-amnioticlipopolysaccharide (LPS)-induced preterm labor/birth that resembles the subclinical syndrome and to compare this model to two established models of LPS-induced preterm labor/birth. METHODS: Pregnant B6 mice received an intra-amniotic, intra-uterine, or intra-peritoneal injection of LPS (100 ng/amniotic sac, 15 μg/25 μL, and 15 μg/200 μL respectively) or PBS (control). Following injection, body temperature (every two hours for a 12-h period), gestational age, and the rate of preterm labor/birth were recorded. RESULTS: An intra-amniotic injection of LPS resulted in preterm labor/birth [LPS 80 ± 24.79% (8/10) versus PBS 0% (0/8); p = 0.001] without causing maternal hypothermia. Intra-peritoneal [LPS 100% (8/8) versus PBS 0% (0/8); p < 0.001)] and intra-uterine [LPS 100% (8/8) versus PBS 28.57 ± 33.47% (2/7); p =0 .007] injections of LPS induced preterm labor/birth; yet, maternal hypothermia was observed. CONCLUSION:Intra-amniotic injection of LPS induces preterm labor/birth in the absence of a body temperature change, which resembles the subclinical syndrome.
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