Amniotic Fluid Interleukin-1 Beta and Interleukin-6, but not Interleukin-8 Correlate with Microbial Invasion of the Amniotic Cavity in Preterm Labor

Marconi, Camila; Ramos, Bruna Ribeiro de Andrade; Peraçoli, José Carlos; Donders, Gilbert; Silva, Márcia Guimarães da

doi:10.1111/j.1600-0897.2010.00940.x

Cited by 89 publications

(70 citation statements)

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“…This decline in T regulatory cells may be permissive of the inflammatory phenomenon reported in the ileum. The latter observation is relevant to the human fetus, because we [77,79] and others [202–205] have previously demonstrated not only the presence of endotoxin in patients with preterm labor, but also increased concentrations of IL-1β [128,131] and IL-1α [128,131] in the amniotic fluid of patients in preterm labor (and in some cases, term labor).…”

Section: Discussionmentioning

confidence: 97%

Bacteria and endotoxin in meconium-stained amniotic fluid at term: could intra-amniotic infection cause meconium passage?

Romero

Yoon

Chaemsaithong

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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Background Meconium-stained amniotic fluid (MSAF) is a common occurrence among women in spontaneous labor at term, and has been associated with adverse outcomes in both mother and neonate. MSAF is a risk factor for microbial invasion of the amniotic cavity (MIAC) and preterm birth among women with preterm labor and intact membranes. We now report the frequency of MIAC and the presence of bacterial endotoxin in the amniotic fluid of patients with MSAF at term. Materials and methods We conducted a cross-sectional study including women in presumed preterm labor because of uncertain dates who underwent amniocentesis, and were later determined to be at term (n=108). Patients were allocated into two groups: (1) MSAF (n=66) and (2) clear amniotic fluid (n=42). The presence of bacteria was determined by microbiologic techniques, and endotoxin was detected using the Limulus amebocyte lysate (LAL) gel clot assay. Statistical analyses were performed to test for normality and bivariate comparisons. Results Bacteria were more frequently present in patients with MSAF compared to those with clear amniotic fluid [19.6% (13/66) versus 4.7% (2/42); p<0.05]. The microorganisms were Gram-negative rods (n=7), Ureaplasma urealyticum (n=4), Gram-positive rods (n=2) and Mycoplasma hominis (n=1). The LAL gel clot assay was positive in 46.9% (31/66) of patients with MSAF, and in 4.7% (2/42) of those with clear amniotic fluid (p <0.001). After heat treatment, the frequency of a positive LAL gel clot assay remained higher in the MSAF group [18.1% (12/66) versus 2.3% (1/42), p<0.05]. Median amniotic fluid IL-6 concentration (ng/mL) was higher [1.3 (0.7–1.9) versus 0.6 (0.3–1.2), p=0.04], and median amniotic fluid glucose concentration (mg/dL) was lower [6 (0–8.9) versus 9 (7.4–12.6), p<0.001] in the MSAF group, than in those with clear amniotic fluid. Conclusion MSAF at term was associated with an increased incidence of MIAC. The index of suspicion for an infection-related process in postpartum women and their neonates should be increased in the presence of MSAF.

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Section: Discussionmentioning

confidence: 97%

Bacteria and endotoxin in meconium-stained amniotic fluid at term: could intra-amniotic infection cause meconium passage?

Romero

Yoon

Chaemsaithong

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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“…In cases with intra-amniotic infection/inflammation, monocytes/macrophages are abundant and expressed high levels of IL-1α and IL-1β 69 . These cytokines participate in the process of parturition 176–178 and host response to intra-amniotic infection 176, 178–185 .…”

Section: Discussionmentioning

confidence: 99%

The immunophenotype of amniotic fluid leukocytes in normal and complicated pregnancies

Gomez‐Lopez

Romero

et al. 2018

American J Rep Immunol

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Problem The immune cellular composition of amniotic fluid is poorly understood. Herein, we determined the immunophenotype of amniotic fluid: 1) immune cells during the second and third trimester; 2) T cells and innate lymphoid cells (ILCs); and 3) immune cells during intra-amniotic infection/inflammation. Method of Study Amniotic fluid samples (n=57) were collected from women from 15-40 weeks of gestation without intra-amniotic infection/inflammation. Samples from women with intra-amniotic infection/inflammation were also included (n=9). Peripheral blood mononuclear cells from healthy adults were used as controls (n=3). Immunophenotyping was performed using flow cytometry. Results In the absence of intra-amniotic infection/inflammation, the amniotic fluid contained several immune cell populations from 15-40 weeks. Among these immune cells: 1) T cells and ILCs were greater than B cells and NK cells between 15 to 30 weeks; 2) T cells were most abundant between 15 to 30 weeks; 3) ILCs were most abundant between 15 to 20 weeks; 4) B cells were scarce between 15 to 20 weeks; yet, they increased and were constant after 20 weeks; 5) NK cells were greater between 15 to 30 weeks than at term; 6) ILCs expressed high levels of RORγt, CD161, and CD103 (i.e. Group 3 ILCs); 7) T cells expressed high levels of RORγt; 8) neutrophils increased as gestation progressed; and 9) monocytes/macrophages emerged after 20 weeks and remained constant until term. All of the amniotic fluid immune cells, except ILCs, were increased in the presence of intra-amniotic infection/inflammation. Conclusions The amniotic fluid harbors a diverse immune cellular composition during normal and complicated pregnancies.

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“…IL-1β in fact was one of the first cytokines implicated in the onset of spontaneous preterm labor (Romero, Durum, et al, 1989) and is further supported by the finding that the human decidua produces IL-1β in response to bacteria (Romero, Wu, et al, 1989). IL-1β concentrations are increased in the amniotic fluid of women with preterm labor and infection, and IL-1β is thought to stimulate the production of prostaglandins and initiate intrauterine contractions (Marconi et al, 2011; Nadeau-Vallee et al, 2016). Similarly TNF-α can stimulate prostaglandin production in the intrauterine tissues, and also in response to bacterial components; elevated TNF-α concentrations have also been shown in women with PPROM and intrauterine infection, and increased TNF-α has been identified as a mechanism for bacteria induced preterm birth (Hillier et al, 1993; Romero et al, 2007).…”

Section: Mechanisms Of Preterm Birth: Infection and Inflammationmentioning

confidence: 99%

The Microbiome and Complement Activation: A Mechanistic Model for Preterm Birth

Dunn

Dunlop

Hogue

et al. 2017

Biological Research For Nursing

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Preterm Birth (PTB, < 37 completed weeks' gestation) is one of the leading obstetrical problems in the United States affecting approximately 1 of every 9 births. Even more concerning are the persistent racial disparities in PTB with particularly high rates in African Americans. There are several recognized pathophysiologic pathways to PTB, including infection and/or exaggerated systemic or local inflammation. Intrauterine infection is a causal factor linked to PTB, thought to result most commonly from inflammatory processes triggered by microbial invasion of bacteria ascending from the vaginal microbiome. Trials to treat various infections have shown limited efficacy in reducing PTB risk, suggesting that other complex mechanisms, including those associated with inflammation, may be involved in the relationship between microbes, infection, and PTB. A key mediator of the inflammatory response, and recently shown to be associated with PTB, is the complement system, an innate defense mechanism involved in both normal physiologic processes that occur during pregnancy implantation, as well as processes that promote the elimination of pathogenic microbes. The purpose of this paper is to present a mechanistic model of inflammation-associated PTB, which hypothesizes a relationship between the microbiome and dysregulation of the complement system. Exploring the relationships between the microbial environment and complement biomarkers may elucidate a potentially modifiable biological pathway to preterm birth.

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Amniotic Fluid Interleukin-1 Beta and Interleukin-6, but not Interleukin-8 Correlate with Microbial Invasion of the Amniotic Cavity in Preterm Labor

Abstract: The frequency of intra-amniotic infection, especially M. hominis, in PL women who delivered with 7 days, is high and correlates with high IL-1β and IL-6 levels, but not IL-8.

Cited by 89 publications

References 38 publications

Bacteria and endotoxin in meconium-stained amniotic fluid at term: could intra-amniotic infection cause meconium passage?

Bacteria and endotoxin in meconium-stained amniotic fluid at term: could intra-amniotic infection cause meconium passage?

The immunophenotype of amniotic fluid leukocytes in normal and complicated pregnancies

The Microbiome and Complement Activation: A Mechanistic Model for Preterm Birth

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