Advances in Inflammatory Causes of Preterm Birth

Abstract

Abstract: Preterm birth (PTB) is a common obstetric complications and it is greatly harmful to mothers and fetals. At present, the mechanism of PTB is not clear. The present research shows that the inflammatory response, especially the inflammatory mediators，plays an important role in the initiation of PTB. The inflammatory mediators on one hand promote the synthesis of prostaglandin and induce uterine contractions, on the other hand promote cervical ripening and trigger matrix metalloproteinases to degrade extracellular matrix, reduce toughness of fetal membranes. The combined effect of all above finally cause uterine contraction, cervical ripening, rupture of fetal membranes, leading to PTB. Microbial infection and the oxidative stress, inhibited autophagy can cause inflammation. PM2.5 may induce mild intrauterine inflammation, resulting in PTB. Mechanism of PTB is unknown and this article will review the mechanism from three aspects. They are the related molecules in inflammation-mediated PTB, the biological and non-biological pathways inducing inflammation.

Key words: Premature birth, Fetal membranes, premature rupture, Infection, Cytokines, Nonbiological factor

GENG Qian，CHANG Ying，CHEN Xu. Advances in Inflammatory Causes of Preterm Birth[J]. Journal of International Obstetrics and Gynecology, 2018, 45(1): 19-22.

References

[1]. Harrison MS, Goldenberg RL. Global burden of prematurity [J]. Seminars in fetal & neonatal medicine, 2016,21(2):74-79. [2]. 张小松. 15家城市医疗机构早产发生情况及影响因素分析 [J]. 中华围产医学杂志. 2016,6(19). [3]. Kobayashi H. The entry of fetal and amniotic fluid components into the uterine vessel circulation leads to sterile inflammatory processes during parturition [J].Front in Immunol,2012,321( 3) : 1-6. [4]. Sheikh IA, Ahmad E, Jamal MS, et al. Spontaneous preterm birth and single nucleotide gene polymorphisms: a recent update [J]. BMC genomics.2016,17(Suppl 9):759. [5]. Romero R, Espinoza J, Goncalves LF, et al. The role of inflammation and infection in preterm birth [J]. Seminars in reproductive medicine. 2007,25(1):21-39. [6]. Wei SQ, Fraser W, Luo ZC. Inflammatory cytokines and spontaneous preterm birth in asymptomatic women: a systematic review [J]. Obstetrics and gynecology.2010,116(2 Pt 1):393-401. [7]. Yin N, Wang H, Zhang H, et al. IL-27 induces a pro-inflammatory response in human fetal membranes mediating preterm birth [J]. International immunopharmacology. 2017,50:361-369. [8]. Kurokawa CS, Hashimoto M, de Souza Rugolo LM, et al. Cord blood cytokine levels in focal early-onset neonatal infection after preterm premature rupture of membranes [J]. The Turkish journal of pediatrics.2013,55(6):598-605. [9]. Nadeau-Vallee M, Obari D, Quiniou C, et al. A critical role of interleukin-1 in preterm labor [J]. Cytokine & growth factor reviews. 2016,28:37-51. [10]. Otsubo Y, Hashimoto K, Kanbe T, et al. Association of cord blood chemokines and other biomarkers with neonatal complications following intrauterine inflammation [J]. PloS one. 2017,12(5):e0175082. [11]. Boyle AK, Rinaldi SF, Norman JE, et al. Preterm birth: Inflammation, fetal injury and treatment strategies [J]. Journal of reproductive immunology. 2017,119:62-66. [12]. Prearo Moco N, Camargo Batista RA, Fernandes Martin L, et al. Toll-Like Receptor-2 and -4 Expression by Maternal Neutrophils in Preterm Labor [J]. Gynecologic and obstetric investigation. 2017. [13]. Karody V,?Reese S,?Kumar N, et al.A toll-like receptor 9 (rs352140) variant is associated with placental inflammation in newborn infants [J].J Matern Fetal Neonatal Med.?2016,29(13):2210-6. [14]. Myntti T, Rahkonen L, Nupponen I, et al. Amniotic Fluid Infection in Preterm Pregnancies with Intact Membranes [J]. Disease markers. 2017,2017:8167276. [15]. Allen TK, Feng L, Grotegut CA, et al. Progesterone receptor membrane component 1 as the mediator of the inhibitory effect of progestins on cytokine-induced matrix metalloproteinase 9 activity in vitro [J]. Reproductive sciences (Thousand Oaks, Calif.). 2014,21(2):260-268. [16]. Tency I, Verstraelen H, Kroes I, et al. Imbalances between matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) in maternal serum during preterm labor [J]. PloS one. 2012,7(11):e49042. [17]. Lai YJ, Hsu TY, Lan KC, et al. Asymptomatic pyuria in pregnant women during the first trimester is associated with an increased risk of adverse obstetrical outcomes [J]. Taiwanese journal of obstetrics & gynecology. 2017,56(2):192-195. [18]. Ren H, Du M. Role of Maternal Periodontitis in Preterm Birth [J]. Frontiers in immunology. 2017,8:139. [19]. Iheozor-Ejiofor Z, Middleton P, Esposito M, et al. Treating periodontal disease for preventing adverse birth outcomes in pregnant women [J]. The Cochrane database of systematic reviews. 2017,6:Cd005297. [20]. Ilhan N, Aygun BK, Gungor H. The relationship between the latency period, infection markers, and oxidant and antioxidant states in women with preterm premature rupture of membranes [J]. Irish journal of medical science. 2017. [21]. de Andrade Ramos BR, Witkin SS. The influence of oxidative stress and autophagy cross regulation on pregnancy outcome [J]. Cell stress & chaperones. 2016,21(5):755-762. [22]. Behnia F, Sheller S, Menon R. Mechanistic Differences Leading to Infectious and Sterile Inflammation [J]. American journal of reproductive immunology (New York, N.Y. : 1989). 2016,75(5):505-518. [23]. 邱其周. 孕妇孕期被动吸烟对母体血浆P-LAP、IL-6及IL-10的影响 [J]. 中国妇幼健康研究. 2017,1(28). [24]. Dutta EH, Behnia F, Boldogh I, et al. Oxidative stress damage-associated molecular signaling pathways differentiate spontaneous preterm birth and preterm premature rupture of the membranes [J]. Molecular human reproduction. 2016,22(2):143-157. [25]. Henkler F, Brinkmann J, Luch A. The role of oxidative stress in carcinogenesis induced by metals and xenobiotics [J]. Cancers. 08 2010;2(2):376-396. [26]. Menon R. Oxidative stress damage as a detrimental factor in preterm birth pathology [J]. Frontiers in immunology. 2014,5:567. [27]. Agrawal V, Jaiswal MK, Mallers T, et al. Altered autophagic flux enhances inflammatory responses during inflammation-induced preterm labor [J]. Scientific reports.2015,5:9410. [28]. Gawriluk TR, Rucker EB. BECN1, corpus luteum function, and preterm labor [J]. Autophagy. 2015,11(1):183-184. [29]. Institute of Medicine Committee on Understanding Premature B, Assuring Healthy O. The National Academies Collection: Reports funded by National Institutes of Health. In: Behrman RE, Butler AS, eds. Preterm Birth: Causes, Consequences, and Prevention [J]. Washington (DC): National Academies Press (US), National Academy of Sciences.2007. [30]. Lee SM, Park KH, Jung EY, et al. Frequency and clinical significance of short cervix in patients with preterm premature rupture of membranes [J]. PloS one. 2017,12(3):e0174657. [31]. Malley CS, Kuylenstierna JC, Vallack HW, et al. Preterm birth associated with maternal fine particulate matter exposure: A global, regional and national assessment [J]. Environment international. 2017,101:173-182. [32]. Nachman RM, Mao G, Zhang X, et al. Intrauterine Inflammation and Maternal Exposure to Ambient PM2.5 during Preconception and Specific Periods of Pregnancy: The Boston Birth Cohort [J]. Environmental health perspectives. 2016,124(10):1608-1615.