Cytokines of the Placenta and Extra-placental Membranes: Roles and Regulation During Human Pregnancy and Parturition

Bowen, J.M.; Chamley, Larry; Keelan, Jeffrey A.; Mitchell, Murray D.

doi:10.1053/plac.2001.0782

Cited by 300 publications

(233 citation statements)

References 251 publications

Supporting

Mentioning

216

Contrasting

Unclassified

Order By: Relevance

“…Similarly, proinflammatory cytokines have also been found in serum/plasma collected from healthy pregnant sows [59] as well as pregnant women [4,24,57]. The proinflammatory cytokines have been proposed to play a physiological role at parturition by being involved in the regulation of the parturition as such [13,29]. Also, cytokines appear to be an important component of a paracrine/autocrine communication network in the mammary gland at different stages of pregnancy and parturition [25,44].…”

Section: Discussionmentioning

confidence: 99%

Morphometric analysis of proinflammatory cytokines in mammary glands of sows suggests an association between clinical mastitis and local production of IL-1beta, IL-6 and TNF-alpha

et al. 2007

View full text Add to dashboard Cite

-Twelve healthy primiparous sows received intramammary inoculation with Escherichia coli (serotype O127) during the 24-h period preceding parturition. Mammary gland biopsy samples were taken immediately before inoculation (0 h) and from the inoculated and the contralateral noninoculated glands 24 h after inoculation. The analyses of interleukin-1 beta (IL-1β), IL-6, IL-8, and tumor necrosis factor alpha (TNF-α) by immunohistochemistry revealed that the production of these proinflammatory cytokines significantly increased in the inoculated mammary glands of sows that developed clinical signs of mastitis (affected group, n = 4) 24 h after inoculation. This was also true for IL-8 in the inoculated mammary glands of sows that did not develop clinical signs of mastitis (nonaffected group, n = 8). Sows that developed clinical signs of mastitis displayed significantly lower constitutive production of IL-1β than did sows that remained clinically healthy. The data indicate that the development of clinical symptoms of coliform mastitis in the sow is associated with a locally increased proinflammatory cytokine production in response to intramammary E. coli infection.cytokine / immunohistochemistry / mastitis / pig / E. coli

show abstract

Section: Discussionmentioning

confidence: 99%

Morphometric analysis of proinflammatory cytokines in mammary glands of sows suggests an association between clinical mastitis and local production of IL-1beta, IL-6 and TNF-alpha

et al. 2007

View full text Add to dashboard Cite

show abstract

“…It induces basal and store-operated calcium entry in myometrial smooth muscle cells (Tribe et al 2003), thus directly enhancing their contractile potential. IL1B can also increase the production of pro-inflammatory cytokines and chemokines; promote the production of prostaglandins via PTGS2, mediators of uterine contractions; and matrix metalloproteinases (MMPs) which activate cervical ripening and foetal membrane rupture, events culminating in successful labour and delivery (Roh et al 2000, Bowen et al 2002, Keelan et al 2003, Lappas & Rice 2004, Christiaens et al 2008, Tattersall, et al 2008. The findings of this study demonstrate that RAF1 is involved in the genesis of pro-inflammatory and RAF1 and labour in myometrium pro-labour mediators induced by IL1B.…”

Section: Discussionmentioning

confidence: 79%

“…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%

“…TNF is another pro-inflammatory cytokine that plays a central role in the terminal effector pathways of human labour and deliver. 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).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

RAF1 is increased in labouring myometrium and modulates inflammation-induced pro-labour mediators

Lappas¹

2016

Reproduction

View full text Add to dashboard Cite

Inflammation plays a central role in the terminal process of human labour and delivery, including myometrial contractions. RAF1 protooncogene serine/threonine-protein kinase (RAF1) can activate ERK (official gene symbol MAPK1) and/or nuclear factor-kappa B (NF-kB) to regulate genes involved in inflammation. There are, however, no studies on the role of RAF1 in the processes of human labour and delivery. Thus, the aims of this study were to determine the effect of i) human labour and pro-inflammatory cytokines interleukin 1 beta (IL1B) and tumour necrosis factor (TNF) alpha on RAF1 protein expression in myometrium and ii) siRNA knockdown of RAF1 on proinflammatory and pro-labour mediators in human myometrial primary cells. Term labour was associated with an increase in RAF1 protein expression. Furthermore, RAF1 protein expression was increased in myometrial cells treated with IL1B and TNF, two likely factors contributing to preterm birth. Knockdown of RAF1 by siRNA in primary myometrial cells significantly decreased IL1B-and TNF-induced IL1A, IL1B, IL6, (C-X-C motif) ligand 8 (CXCL8)and chemokine (C-C motif) ligand 2 (CCL2) mRNA abundance and IL6, IL8 and CCL2; prostaglandin-endoperoxide synthase 2 (PTGS2) mRNA levels and prostaglandin PGF 2a release; and NF-kB activation. Furthermore, RAF1 knockdown was associated with decreased activation of ERK in the presence of IL1B but not TNF. Concordantly, the ERK inhibitor U0126 significantly decreased IL1B-induced IL6, CXCL8, CCL2 and PTGS2 mRNA abundance; IL6, CXCL8, CCL2 and PGF 2a release; and NF-kB activation. In conclusion, IL1B induces the expression and secretion of pro-labour mediators through the RAF1-MAPK1-NF-kB signalling pathway. TNF, on the other hand, regulates pro-labour mediators through the RAF1-NF-kB signalling pathway via an MAPK1-independent mechanism.

show abstract

“…Cytokines produced by cells in the feto-maternal interface play a key role in the regulation of placental development (i.e., trophoblast proliferation, migration, and invasion) and function (i.e., placental hormone secretion) (Bowen et al 2002). Nicotine treatment of placental cells in vitro reduced lipopolysaccharide (LPS)-induced production of the cytokines IL1b and IL6 (Dowling et al 2007), which play an important role in trophoblast invasion and migration (Jovanovic & Vicovac 2009, Prutsch et al 2012.…”

Section: The Role Of Inflammationmentioning

confidence: 99%

Adverse effects of perinatal nicotine exposure on reproductive outcomes

Wong¹,

Barra²,

Alfaidy³

et al. 2015

Reproduction

View full text Add to dashboard Cite

Nicotine exposure during pregnancy through cigarette smoking, nicotine replacement therapies or e-cigarette use continues to be a widespread public health problem, impacting both fetal and postnatal health. Yet, at this time, there remains limited data regarding the safety and efficacy in using these nicotine products during pregnancy. Notably, reports assessing the effect of nicotine exposure on postnatal health outcomes in humans, including reproductive health, are severely lacking. Our current understanding regarding the consequences of nicotine exposure during pregnancy is limited to a few animal studies, which do not comprehensively address the underlying cellular mechanisms involved. This paper aims to critically review the current knowledge from human and animal studies regarding the direct and indirect effects (e.g. obesity) of maternal nicotine exposure, regardless of its source, on reproductive outcomes in pregnancy and postnatal life. Furthermore, this review highlights several key cellular mechanisms involved in these adverse reproductive deficits including oxidative stress, inflammation, and endoplasmic reticulum (ER) stress. By understanding the interplay of the cellular mechanisms involved, further strategies could be developed to prevent the reproductive abnormalities resulting from exposure to nicotine in utero and influence informed clinical guidelines for pregnant women.Reproduction (2015) 150 R185-R193

show abstract

Cytokines of the Placenta and Extra-placental Membranes: Roles and Regulation During Human Pregnancy and Parturition

Cited by 300 publications

References 251 publications

Morphometric analysis of proinflammatory cytokines in mammary glands of sows suggests an association between clinical mastitis and local production of IL-1beta, IL-6 and TNF-alpha

Morphometric analysis of proinflammatory cytokines in mammary glands of sows suggests an association between clinical mastitis and local production of IL-1beta, IL-6 and TNF-alpha

RAF1 is increased in labouring myometrium and modulates inflammation-induced pro-labour mediators

Adverse effects of perinatal nicotine exposure on reproductive outcomes

Contact Info

Product

Resources

About