Interleukin-10 in amniotic fluid at midtrimester: Immune activation and suppression in relation to fetal growth

Heyborne, Kent; McGregor, James A.; Henry, George P.; Witkin, Steven S.; Abrams, John S.

doi:10.1016/s0002-9378(94)70077-x

Cited by 79 publications

(49 citation statements)

References 19 publications

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“…The lack of benefit of IL-10 treatment for fetal mass contrasts with previous experiments in rats where LPS-induced fetal growth restriction was alleviated with exogenous IL-10 supplied at similar doses (28,29). However, consistent with our findings, human clinical studies link elevated placental and amniotic IL-10 synthesis with in utero growth restriction (61).…”

Section: Discussionsupporting

confidence: 71%

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Robertson

Skinner

Care

2006

The Journal of Immunology

174

139

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IL-10 is highly expressed in the uterus and placenta and is implicated in controlling inflammation-induced pathologies of pregnancy. To investigate the role of IL-10 in regulating preterm labor, the response of IL-10 null mutant mice to low-dose LPS in late gestation was evaluated. When IL-10 null mutant C57BL/6 (IL-10−/−) and control (IL-10+/+) mice were administered LPS on day 17 of pregnancy, the dose of LPS required to elicit 50% preterm fetal loss was 10-fold lower in IL-10−/− mice than in IL-10+/+ mice. Surviving fetuses in IL-10−/− mice exhibited fetal growth restriction at lower doses of LPS than IL-10+/+ mice. Marked elevation of LPS-induced immunoactive TNF-α and IL-6 was evident in the serum, uterus, and placenta of IL-10−/− mice, and TNF-α and IL-6 mRNA expression was elevated in the uterus and placenta, but not the fetus. Serum IL-1α, IFN-γ, and IL-12p40 were increased and soluble TNFRII was diminished in the absence of IL-10, with these changes also reflected in the gestational tissues. Administration of rIL-10 to IL-10−/− mice attenuated proinflammatory cytokine synthesis and alleviated their increased susceptibility to preterm loss. Exogenous IL-10 also protected IL-10+/+ mice from fetal loss. These data show that IL-10 modulates resistance to inflammatory stimuli by down-regulating proinflammatory cytokines in the uterus and placenta. Abundance of endogenous IL-10 in gestational tissues is therefore identified as a critical determinant of resistance to preterm labor, and IL-10 may provide a useful therapeutic agent in this common condition.

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Section: Discussionsupporting

confidence: 71%

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Robertson

Skinner

Care

2006

The Journal of Immunology

174

139

View full text Add to dashboard Cite

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“…Dysregulation of anti-inflammatory mediators has also been reported in these pathologies. IL10 levels are elevated in amniotic fluid at mid-trimester in women with intrauterine growth restriction and elevated in term placenta in women with preeclampsia (Heyborne et al 1994, Rinehart et al 1999. IL10 has also been reported to be aberrantly expressed in decidual T lymphocytes in women with recurrent miscarriage (Piccinni et al 1998).…”

Section: Inflammatory Pathways In Reproductive Pathologymentioning

confidence: 99%

Inflammatory pathways in female reproductive health and disease

Jabbour¹,

Sales²,

Catalano³

et al. 2009

Reproduction

291

226

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Inflammation involves alterations to vascular and immune cell function. It is well recognised that many physiological reproductive events such as ovulation, menstruation, implantation and onset of labour display hallmark signs of inflammation. These are orchestrated by specific molecular pathways involving a host of growth factors, cytokines, chemokines and lipid mediators. Resumption of normal reproductive function involves prompt and proper resolution of these inflammatory pathways. Recent literature confirms that resolution of inflammatory pathways involves specific biochemical events that are activated to re-establish homeostasis in the affected tissue. Moreover, initiation and maintenance of inflammatory pathways are the key components of many pathologies of the reproductive tract and elsewhere in the body. The onset of reproductive disorders or disease may be the result of exacerbated activation and maintenance of inflammatory pathways or their dysregulated resolution. This review will address the role of inflammatory events in normal reproductive function and its pathologies.

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“…Inversely, failure to mount a local inflammatory response in early or late gestation can also lead to adverse conditions, including miscarriages. Evidence shows that impaired inflammatory response is implicated in numerous female reproductive tract pathologies including menstrual disorders (Sales & Jabbour 2003), endometriosis-associated infertility (Gupta et al 2008), recurrent miscarriage (von Wolff et al 2000, Laird et al 2003, intrauterine growth restriction (Heyborne et al 1994), preeclampsia , Rinehart et al 1999) and preterm labor (Romero et al 2006. Infertility has an estimated global prevalence of 9% with >72 million infertile women worldwide (Boivin et al 2007), whereas preterm birth and preeclampsia, the two leading causes of perinatal mortality and morbidity, have an estimated prevalence of >11% (Blencowe et al 2013) and 3-5% (Ananth et al 2013 respectively.…”

Section: Introductionmentioning

confidence: 99%

Sterile inflammation and pregnancy complications: a review

Nadeau-Vallée¹,

Obari²,

Palacios³

et al. 2016

Reproduction

213

161

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Inflammation is essential for successful embryo implantation, pregnancy maintenance and delivery. In the last decade, important advances have been made in regard to endogenous, and therefore non-infectious, initiators of inflammation, which can act through the same receptors as pathogens. These molecules are referred to as damage-associated molecular patterns (DAMPs), and their involvement in reproduction has only recently been unraveled. Even though inflammation is necessary for successful reproduction, untimely activation of inflammatory processes can have devastating effect on pregnancy outcomes. Many DAMPs, such as uric acid, high-mobility group box 1 (HMGB1), interleukin (IL)-1 and cell-free fetal DNA, have been associated with pregnancy complications, such as miscarriages, preeclampsia and preterm birth in preclinical models and in humans. However, the specific contribution of alarmins to these conditions is still under debate, as currently there is lack of information on their mechanism of action. In this review, we discuss the role of sterile inflammation in reproduction, including early implantation and pregnancy complications. Particularly, we focus on major alarmins vastly implicated in numerous sterile inflammatory processes, such as uric acid, HMGB1, IL-1α and cell-free DNA (especially that of fetal origin) while giving an overview of the potential role of other candidate alarmins.Reproduction (2016) 152 R277-R292

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Interleukin-10 in amniotic fluid at midtrimester: Immune activation and suppression in relation to fetal growth

Cited by 79 publications

References 19 publications

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Inflammatory pathways in female reproductive health and disease

Sterile inflammation and pregnancy complications: a review

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