2006
DOI: 10.1016/j.ajog.2006.06.072
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Preterm labor is induced by intraamniotic infusions of interleukin-1β and tumor necrosis factor-α but not by interleukin-6 or interleukin-8 in a nonhuman primate model

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Cited by 308 publications
(245 citation statements)
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“…(1) stimulation of IL-1R induces the transcription of numerous pro-labor genes via MAPK p38, JNK, c-jun and small GTPase Rho in myometrial smooth muscle cells, which results in increased myometrial contractility (Tribe et al 2003, Chevillard et al 2007, Nadeau-Vallee et al 2015b; and preterm labor in mice and non-human primates (Romero et al 1991, Sadowsky et al 2006; (2) antagonism of IL-1R prevents all of these events (Romero & Tartakovsky 1992, Nadeau-Vallee et al 2015b; (3) IL-1α amniotic fluid levels are elevated in women that deliver preterm (Figueroa et al 2005); (4) preterm labor is associated with increased IL-1α activity in amniotic fluids (Romero et al 1989); and (5) maternal polymorphisms and haplotypes in the IL-1α gene (Sata et al 2009), as well as fetal polymorphism in the endogenous IL-1R antagonist (Witkin et al 2003), have been associated with increased risk of preterm birth. The critical role of IL-1 in preterm labor has been reviewed elsewhere (Nadeau-Vallee et al 2015a).…”
Section: Preterm Labormentioning
confidence: 99%
“…(1) stimulation of IL-1R induces the transcription of numerous pro-labor genes via MAPK p38, JNK, c-jun and small GTPase Rho in myometrial smooth muscle cells, which results in increased myometrial contractility (Tribe et al 2003, Chevillard et al 2007, Nadeau-Vallee et al 2015b; and preterm labor in mice and non-human primates (Romero et al 1991, Sadowsky et al 2006; (2) antagonism of IL-1R prevents all of these events (Romero & Tartakovsky 1992, Nadeau-Vallee et al 2015b; (3) IL-1α amniotic fluid levels are elevated in women that deliver preterm (Figueroa et al 2005); (4) preterm labor is associated with increased IL-1α activity in amniotic fluids (Romero et al 1989); and (5) maternal polymorphisms and haplotypes in the IL-1α gene (Sata et al 2009), as well as fetal polymorphism in the endogenous IL-1R antagonist (Witkin et al 2003), have been associated with increased risk of preterm birth. The critical role of IL-1 in preterm labor has been reviewed elsewhere (Nadeau-Vallee et al 2015a).…”
Section: Preterm Labormentioning
confidence: 99%
“…TNF can amplify or initiate the process of parturition by further increasing cytokine production, increasing PTGS2-mediated prostaglandin synthesis and activating MMPs (Roh et al 2000, Bowen et al 2002, Keelan et al 2003, Lappas & Rice 2004, Christiaens et al 2008, Tattersall et al 2008. In addition, TNF can induce preterm labour in animal models (Sadowsky et al 2006). Thus, it was also of interest to determine if RAF1 also regulates pro-inflammatory and pro-labour mediators in the presence of TNF.…”
Section: Discussionmentioning
confidence: 99%
“…Human labour is associated with increased concentrations of IL1B in both gestational tissues and biological fluids (Elliott, et al 2001, Bowen et al 2002, Tattersall et al 2008, and intra-amniotic and/or systemic administration of IL1B to mice and monkeys induces preterm labour (Romero et al 1991, Romero & Tartakovsky 1992, Sadowsky et al 2006. IL1B is thought to contribute to the onset of labour by stimulating and potentiating uterine contractions.…”
Section: Discussionmentioning
confidence: 99%
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“…In contrast to the sheep model, amniotic fluid inoculation with Ureaplasma in the Rhesus model at ϳ75% gestation results in a progressive increase in uterine contractility culminating in preterm labor, suggesting a unique species difference in host response (52,65). Nearly 80% of preterm births occurred within 1 wk of inoculation and all occurred within 15 days.…”
Section: Ureaplasma Modelmentioning
confidence: 99%