The potential role of prolactin as a modulator of the secretion of proinflammatory mediators in chorioamniotic membranes in term human gestation

Zaga‐Clavellina, Veronica; Parra-Covarrubias, A; Ramírez-Peredo, Jorge; Vega-Sánchez, Rodrigo; Vadillo-Ortega, Felipe

doi:10.1016/j.ajog.2014.01.039

Cited by 15 publications

(9 citation statements)

References 24 publications

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“…Similar uncertainty exists around the anti-inflammatory effects we observed with prolactin which attenuated the amount of IL-1β produced by CBMCs, PLBCs, MBMCs, and fetal membranes costimulated with LPS and BzATP. A recent finding also noted inhibition of IL-1β in fetal membranes by prolactin but over a much longer time course of 32 h (Zaga-Clavellina et al, 2014 ). Addition of LPS activated the synthesis of prolactin receptor mRNA and prolactin mRNA in human monocytes in vitro up to 300- and 130-fold, respectively (Lopez-Rincon et al, 2013 ) and is interesting in the context that human decidua produces large amounts of prolactin throughout pregnancy (Rosenberg et al, 1980 ), that like P4, may play a role in local host-defense responses.…”

Section: Discussionmentioning

confidence: 89%

Caspase-1-mediated cytokine release from gestational tissues, placental, and cord blood

et al. 2015

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Distinguishing between fetal and maternal inflammatory responses is necessary for understanding the immune interplay either side of the placenta. Fetal immunity reaches maturity during extrauterine life and while basic inflammatory responses afford a certain degree of protection, fetuses are vulnerable to infection. With the discovery of inflammasomes—intracellular scaffolds that facilitate the elaboration of reactions resulting in the release of mature interleukin-1β (IL-1β)—it is necessary to consider how inflammatory stimuli are processed. The purinergic P2X7 receptor located on haematopoietic cells is a key intermediary in signal transduction initiated at Toll-like receptors (TLR) terminating in release of the mature IL-1β product. We demonstrate herein that IL-1β release from fetal membranes and mononuclear cells isolated from cord, placental, and maternal blood, obtained at term, is P2X7- and caspase-1 dependent. The P2X7-dependent release of the cytokine, which was highest from choriodecidua, was attenuated by progesterone (P4), prolactin and an NFkB inhibitor. The NLRP3 inflammasome appears necessary for the processing of IL-1β in gestational tissues and leukocytes.

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Section: Discussionmentioning

confidence: 89%

Caspase-1-mediated cytokine release from gestational tissues, placental, and cord blood

et al. 2015

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“…For instance, PRL treatment was shown to induce interleukin (IL)-1β, gamma interferon and tumour necrosis factor (TNF)-α release by murine peritoneal macrophages in vitro (Sodhi and Tripathi, 2008). In contrast, our laboratory demonstrated that exogenous PRL downregulated IL-1β and TNF-α in cultured chorioamniotic membranes (Zaga-Clavellina et al , 2014; Flores-Espinosa et al , 2017). Taking into account the PRL-R and PRL expression in placenta, it is critical to understand the regulation of the placental immune profile by this hormone, especially under an inflammatory scenario.…”

Section: Introductionmentioning

confidence: 74%

Prolactin decreases LPS-induced inflammatory cytokines by inhibiting TLR-4/NFκB signaling in the human placenta

Olmos-Ortíz

Déciga-García

Preciado-Martínez

et al. 2019

Molecular Human Reproduction

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Prolactin (PRL) plays an important role in trophoblast growth, placental angiogenesis and immunomodulation within the feto-maternal interface, where different cell types secrete PRL and express its receptor. During pregnancy, inflammatory signalling is a deleterious event that has been associated with poor fetal outcomes. The placenta is highly responsive to the inflammatory stimulus; however, the actions of PRL in placental immunity and inflammation remain largely unknown. The aim of this study was to evaluate PRL effects on the TLR4/NFkB signalling cascade and associated inflammatory targets in cultured explants from healthy term human placentas. An in utero inflammatory scenario was mimicked using lipopolysaccharides (LPS) from Escherichia coli. PRL significantly reduced LPS-dependent TNF-α, IL-1β and IL-6 secretion and intracellular levels. Mechanistically, PRL prevented LPS-mediated upregulation of TLR-4 expression and NFκB phosphorylation. In conclusion, PRL limited inflammatory responses to LPS in the human placenta, suggesting that this hormone could be critical in inhibiting exacerbated immune responses to infections that could threaten pregnancy outcome. This is the first evidence of a mechanism for anti-inflammatory activity of PRL in the human placenta, acting as a negative regulator of TLR-4/NFkB signaling.

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“…The overall consensus was an increase in TNF-α protein. 23, 25, 46, 59, 60,61 and an increase in TNF-α mRNA 27, 28, 33, 55, 58, 60, 61 at the time of term labor or when labor was simulated in vitro . Interestingly, Alexander et al 2012 found that TNF-α 1A receptor mRNA increases in the myometrium with labor.…”

Section: Discussionmentioning

confidence: 99%

“…IL-1β is an inflammatory mediator that can induce the production of other pro-labor mediators. 22, 60, 62, 86 IL-1β promotes adhesion of white blood cells by increasing expression of adhesion molecules. 25 Our review found 19 articles that reported on IL-1β.…”

Section: Discussionmentioning

confidence: 99%

Gestational tissue inflammatory biomarkers at term labor: A systematic review of literature

Hadley

Richardson

Torloni

et al. 2017

American J Rep Immunol

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Parturition at term is characterized by inflammatory overload in both feto-maternal tissues. Despite the large number of individual studies on changes in inflammatory biomarkers linked to labor, a comprehensive profile of them in each of the uterine compartments is not available to better understand their mechanistic contributions to labor. This systematic review investigated the pro- and anti-inflammatory biomarkers reported in intra-uterine tissues (amnion, chorion, decidua, placenta, and myometrium) at term labor. We conducted a systematic review of studies on pro- and anti-inflammatory biomarkers (mRNA and/or protein) reported in feto-maternal tissues during normal human term labor, published in English (1980-2016), in 3 electronic data bases. From a total of 3712 citations, 172 were included for final review. Each tissue expresses a unique set of biomarkers at the time of term labor, but there is significant overlap between tissues. All tissues had IL-6, IL-8, IL-1β, COX-2, PGE-2, TNF-α, and hCAP18 in common at term labor. Common and unique inflammatory biomarkers are expressed in various feto-maternal compartments at term labor. Increase in pro-inflammatory markers in all gestational tissue signifies their harmonious functional role in promoting labor. Anti-inflammatory markers at term labor are hardly reported.

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The potential role of prolactin as a modulator of the secretion of proinflammatory mediators in chorioamniotic membranes in term human gestation

Cited by 15 publications

References 24 publications

Caspase-1-mediated cytokine release from gestational tissues, placental, and cord blood

Caspase-1-mediated cytokine release from gestational tissues, placental, and cord blood

Prolactin decreases LPS-induced inflammatory cytokines by inhibiting TLR-4/NFκB signaling in the human placenta

Gestational tissue inflammatory biomarkers at term labor: A systematic review of literature

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