Fetal Membrane Inflammation Induces Preterm Birth Via Toll-Like Receptor 2 in Mice With Chronic Gingivitis

Inflammation is associated with preterm birth. We previously described a mouse model of chronic inflammation-induced preterm birth after dental Porphyromonas gingivalis infection. The aim of this study was to employ this model system to investigate the mechanisms through which enhanced uterine contr...

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Veröffentlicht in:Reproductive sciences (Thousand Oaks, Calif.) Calif.), 2019-07, Vol.26 (7), p.869-878
Hauptverfasser: Konishi, Haruhisa, Urabe, Satoshi, Miyoshi, Hiroshi, Teraoka, Yuko, Maki, Tomoko, Furusho, Hisako, Miyauchi, Mutsumi, Takata, Takashi, Kudo, Yoshiki, Kajioka, Shunichi
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container_issue 7
container_start_page 869
container_title Reproductive sciences (Thousand Oaks, Calif.)
container_volume 26
creator Konishi, Haruhisa
Urabe, Satoshi
Miyoshi, Hiroshi
Teraoka, Yuko
Maki, Tomoko
Furusho, Hisako
Miyauchi, Mutsumi
Takata, Takashi
Kudo, Yoshiki
Kajioka, Shunichi
description Inflammation is associated with preterm birth. We previously described a mouse model of chronic inflammation-induced preterm birth after dental Porphyromonas gingivalis infection. The aim of this study was to employ this model system to investigate the mechanisms through which enhanced uterine contractility induces preterm birth. Messenger RNA (mRNA) encoding contraction-associated proteins, such as oxytocin receptors, was measured at various gestational time points by real-time polymerase chain reaction (PCR). Spontaneous and oxytocin-induced uterine contractile activity at gestational day 18 was assessed using a tissue organ bath. The expression levels of Toll-like receptor 2 (TLR2), TLR4, cyclooxygenase (COX)-2, nuclear factor-kappa B (NF-κB) p65, and p38 mitogen-activated protein kinase (MAPK) on gestational day 18 were also determined by real-time PCR or Western blotting. Messenger RNA encoding contraction-associated proteins was increased at gestational day 18, and the spontaneous contractile activity (1.6-fold greater area under the contraction curve) and sensitivity to oxytocin (EC50: 8.8 nM vs 2.2 nM) were enhanced in the P gingivalis group compared to those in the control group. In the P gingivalis group, COX-2 mRNA expression was not elevated in the placenta or myometrium but was upregulated 2.3-fold in the fetal membrane. The TLR2 mRNA levels in the fetal membrane were 2.7-fold higher in the P gingivalis group, whereas TLR4 levels were not elevated. Activation of the NF-κB p65 and p38 MAPK pathways was enhanced in the fetal membrane of the P gingivalis group. Thus, in mice with chronic dental P gingivalis infection, TLR2-induced inflammation in the fetal membrane leads to upregulation of uterine contractility, leading to preterm birth.
doi_str_mv 10.1177/1933719118792097
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We previously described a mouse model of chronic inflammation-induced preterm birth after dental Porphyromonas gingivalis infection. The aim of this study was to employ this model system to investigate the mechanisms through which enhanced uterine contractility induces preterm birth. Messenger RNA (mRNA) encoding contraction-associated proteins, such as oxytocin receptors, was measured at various gestational time points by real-time polymerase chain reaction (PCR). Spontaneous and oxytocin-induced uterine contractile activity at gestational day 18 was assessed using a tissue organ bath. The expression levels of Toll-like receptor 2 (TLR2), TLR4, cyclooxygenase (COX)-2, nuclear factor-kappa B (NF-κB) p65, and p38 mitogen-activated protein kinase (MAPK) on gestational day 18 were also determined by real-time PCR or Western blotting. Messenger RNA encoding contraction-associated proteins was increased at gestational day 18, and the spontaneous contractile activity (1.6-fold greater area under the contraction curve) and sensitivity to oxytocin (EC50: 8.8 nM vs 2.2 nM) were enhanced in the P gingivalis group compared to those in the control group. In the P gingivalis group, COX-2 mRNA expression was not elevated in the placenta or myometrium but was upregulated 2.3-fold in the fetal membrane. The TLR2 mRNA levels in the fetal membrane were 2.7-fold higher in the P gingivalis group, whereas TLR4 levels were not elevated. Activation of the NF-κB p65 and p38 MAPK pathways was enhanced in the fetal membrane of the P gingivalis group. 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Sci</addtitle><addtitle>Reprod Sci</addtitle><description>Inflammation is associated with preterm birth. We previously described a mouse model of chronic inflammation-induced preterm birth after dental Porphyromonas gingivalis infection. The aim of this study was to employ this model system to investigate the mechanisms through which enhanced uterine contractility induces preterm birth. Messenger RNA (mRNA) encoding contraction-associated proteins, such as oxytocin receptors, was measured at various gestational time points by real-time polymerase chain reaction (PCR). Spontaneous and oxytocin-induced uterine contractile activity at gestational day 18 was assessed using a tissue organ bath. The expression levels of Toll-like receptor 2 (TLR2), TLR4, cyclooxygenase (COX)-2, nuclear factor-kappa B (NF-κB) p65, and p38 mitogen-activated protein kinase (MAPK) on gestational day 18 were also determined by real-time PCR or Western blotting. 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Public Health</topic><topic>Mice, Inbred C57BL</topic><topic>Obstetrics/Perinatology/Midwifery</topic><topic>Original Article</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Porphyromonas gingivalis - pathogenicity</topic><topic>Pregnancy</topic><topic>Premature Birth - etiology</topic><topic>Premature Birth - immunology</topic><topic>Premature Birth - metabolism</topic><topic>Premature Birth - physiopathology</topic><topic>Reproductive Medicine</topic><topic>Signal Transduction</topic><topic>Toll-Like Receptor 2 - genetics</topic><topic>Toll-Like Receptor 2 - immunology</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Transcription Factor RelA - metabolism</topic><topic>Uterine Contraction</topic><topic>Uterus - immunology</topic><topic>Uterus - metabolism</topic><topic>Uterus - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Konishi, Haruhisa</creatorcontrib><creatorcontrib>Urabe, Satoshi</creatorcontrib><creatorcontrib>Miyoshi, Hiroshi</creatorcontrib><creatorcontrib>Teraoka, Yuko</creatorcontrib><creatorcontrib>Maki, Tomoko</creatorcontrib><creatorcontrib>Furusho, Hisako</creatorcontrib><creatorcontrib>Miyauchi, Mutsumi</creatorcontrib><creatorcontrib>Takata, Takashi</creatorcontrib><creatorcontrib>Kudo, Yoshiki</creatorcontrib><creatorcontrib>Kajioka, Shunichi</creatorcontrib><collection>Springer Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Reproductive sciences (Thousand Oaks, Calif.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Konishi, Haruhisa</au><au>Urabe, Satoshi</au><au>Miyoshi, Hiroshi</au><au>Teraoka, Yuko</au><au>Maki, Tomoko</au><au>Furusho, Hisako</au><au>Miyauchi, Mutsumi</au><au>Takata, Takashi</au><au>Kudo, Yoshiki</au><au>Kajioka, Shunichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fetal Membrane Inflammation Induces Preterm Birth Via Toll-Like Receptor 2 in Mice With Chronic Gingivitis</atitle><jtitle>Reproductive sciences (Thousand Oaks, Calif.)</jtitle><stitle>Reprod. Sci</stitle><addtitle>Reprod Sci</addtitle><date>2019-07-01</date><risdate>2019</risdate><volume>26</volume><issue>7</issue><spage>869</spage><epage>878</epage><pages>869-878</pages><issn>1933-7191</issn><eissn>1933-7205</eissn><abstract>Inflammation is associated with preterm birth. We previously described a mouse model of chronic inflammation-induced preterm birth after dental Porphyromonas gingivalis infection. The aim of this study was to employ this model system to investigate the mechanisms through which enhanced uterine contractility induces preterm birth. Messenger RNA (mRNA) encoding contraction-associated proteins, such as oxytocin receptors, was measured at various gestational time points by real-time polymerase chain reaction (PCR). Spontaneous and oxytocin-induced uterine contractile activity at gestational day 18 was assessed using a tissue organ bath. The expression levels of Toll-like receptor 2 (TLR2), TLR4, cyclooxygenase (COX)-2, nuclear factor-kappa B (NF-κB) p65, and p38 mitogen-activated protein kinase (MAPK) on gestational day 18 were also determined by real-time PCR or Western blotting. Messenger RNA encoding contraction-associated proteins was increased at gestational day 18, and the spontaneous contractile activity (1.6-fold greater area under the contraction curve) and sensitivity to oxytocin (EC50: 8.8 nM vs 2.2 nM) were enhanced in the P gingivalis group compared to those in the control group. In the P gingivalis group, COX-2 mRNA expression was not elevated in the placenta or myometrium but was upregulated 2.3-fold in the fetal membrane. The TLR2 mRNA levels in the fetal membrane were 2.7-fold higher in the P gingivalis group, whereas TLR4 levels were not elevated. Activation of the NF-κB p65 and p38 MAPK pathways was enhanced in the fetal membrane of the P gingivalis group. Thus, in mice with chronic dental P gingivalis infection, TLR2-induced inflammation in the fetal membrane leads to upregulation of uterine contractility, leading to preterm birth.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>30223727</pmid><doi>10.1177/1933719118792097</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Springer Nature; SAGE Journals; Alma/SFX Local Collection
subjects Animals
Chorioamnionitis - etiology
Chorioamnionitis - immunology
Chorioamnionitis - metabolism
Cyclooxygenase 2 - genetics
Cyclooxygenase 2 - metabolism
Disease Models, Animal
Embryology
Extraembryonic Membranes - immunology
Extraembryonic Membranes - metabolism
Female
Gingivitis - complications
Gingivitis - immunology
Gingivitis - metabolism
Gingivitis - microbiology
Medicine & Public Health
Mice, Inbred C57BL
Obstetrics/Perinatology/Midwifery
Original Article
p38 Mitogen-Activated Protein Kinases - metabolism
Porphyromonas gingivalis - pathogenicity
Pregnancy
Premature Birth - etiology
Premature Birth - immunology
Premature Birth - metabolism
Premature Birth - physiopathology
Reproductive Medicine
Signal Transduction
Toll-Like Receptor 2 - genetics
Toll-Like Receptor 2 - immunology
Toll-Like Receptor 2 - metabolism
Transcription Factor RelA - metabolism
Uterine Contraction
Uterus - immunology
Uterus - metabolism
Uterus - physiopathology
title Fetal Membrane Inflammation Induces Preterm Birth Via Toll-Like Receptor 2 in Mice With Chronic Gingivitis
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