Plasma IL-17, IL-35, interferon-γ, SOCS3 and TGF-β levels in pregnant women with preeclampsia, and their relation with severity of disease

Ozkan, Zehra Sema; Şi̇mşek, Mehmet; Ilhan, Fulya; Deveci, Derya; Gödekmerdan, Ahmet; Sapmaz, Ekrem

doi:10.3109/14767058.2013.861415

Cited by 53 publications

(42 citation statements)

References 29 publications

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“…Multiplex bead array technology has a high dynamic range, and it may not be optimal for evaluating analytes with very low concentration. In a recent study, IL-17 levels were determined in plasma samples of 40 preeclamptic and 40 normotensive pregnant women with ELISA (Ozkan et al 2014). The authors found lower IL-17 levels in the preeclamptic group.…”

Section: Discussionmentioning

confidence: 99%

Increased circulating interleukin-17 levels in preeclampsia

Molvarec

Czegle

Szijártó³

et al. 2015

Journal of Reproductive Immunology

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Increasing evidence suggests that an exaggerated maternal systemic inflammatory response, as well as an angiogenic imbalance plays a central role in the pathogenesis of preeclampsia. In this study, we determined circulating levels of interleukin-17 (IL-17) along with those of angiogenic factors in healthy non-pregnant and pregnant women and preeclamptic patients, and examined whether serum IL-17 levels of preeclamptic patients were related to their clinical features and angiogenic factor concentrations. Fifty-nine preeclamptic patients, 60healthy pregnant women and 56 healthy non-pregnant women were involved in this casecontrol study. Serum levels of IL-17A were measured by high sensitivity ELISA. Serum total soluble fms-like tyrosine kinase-1 (sFlt-1) and biologically active placental growth factor (PlGF) levels were determined by electrochemiluminescence immunoassay. For statistical analyses, non-parametric methods were applied. Serum IL-17 levels were significantly higher in preeclamptic patients than in healthy non-pregnant and pregnant women. We did not find any relationship between serum IL-17 concentrations of preeclamptic patients and their clinical features and serum sFlt-1 and PlGF levels or sFlt-1/PlGF ratios. However, elevated serum IL-17 level and sFlt-1/PlGF ratio was found to be additive for the risk of preeclampsia, as shown by the substantially higher odds ratios of their combination than of either alone. In conclusion, serum IL-17 levels are increased in preeclampsia, which might contribute to the development of the excessive systemic inflammatory response characteristic of the maternal syndrome of the disease. In addition, elevated serum IL-17 level and sFlt-1/PlGF ratio had an additive (joint) effect in the risk of preeclampsia.

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Section: Discussionmentioning

confidence: 99%

Increased circulating interleukin-17 levels in preeclampsia

Molvarec

Czegle

Szijártó³

et al. 2015

Journal of Reproductive Immunology

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“…However, it also has an important role in induction of the protective immune response against extracellular bacteria or fungal pathogens at mucosal surfaces (608, 611–623). Th17 cells seem to participate in successful pregnancy processes and can be lower in PE (624–626), although more studies show them as higher (599, 627–635) or unchanged (636, 637). One interpretation, consistent with the present thesis, is that the antimicrobial effects of placental IL-17 relative to T reg cells are compromised during PE (599, 633, 638).…”

Section: Effects Of Lps and Other Microbial Antigens On Disrupting Trmentioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one.

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“…They observed significantly decreased SOCS-3 levels in preeclamptic women compared to that in normotensive controls. Ozkan et al [12] observed negative correlation between maternal plasma SOCS-3 levels and severity of PE. Wang et al [13] reported reduced SOCS-3 expression in leukocyte and vessel endothelium of preeclamptic women compared to those in normotensive pregnants.…”

Section: Are There Any Differences Between Preeclamptic and Healty Prmentioning

confidence: 98%

“…Suppressor of cytokine signaling-3 (SOCS-3) plays an important role in negative regulation of inflammatory response [11]. Decreased serum and placental SOCS-3 levels in preeclampsia may account for the increased inflammatory response in PE [12][13][14]. We hypothesize that both of MFG-E8 and SOCS3 levels may decrease or increase either being result or reason of PE.…”

Section: Introductionmentioning

confidence: 99%

Untitled

2017

OGIJ

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This prospective, cross-sectional study was conducted with 90 pregnant women who were hospitalized at Firat University Hospital, Department of Gynecology and Obstetrics between December 2013 and December 2015 after local ethics committee approval (Decision No: 06/2013). The study population was consisted of 40 preeclampsia pregnant women (study group) and 50 healthy, gestational age matched pregnant women without previous history of PE (control group AbstractPurpose: Preeclampsia (PE) is closely associated with systemic inflammatory response. Milk Fat Globule Epidermal Growth Factor-8 (MFG-E8), an endometrial epithelial protein, regulates inflammation and apoptosis. Suppressor of cytokine signaling-3 (SOCS-3) plays role on prevention of inflammation. We evaluated the serum and placenta levels of MFG-E8 and SOCS-3 in preeclampsia and healthy pregnant women. Methods:The study population was consisted of 40 preeclampsia and 50 healthy, gestational-age matched women with no history of preeclampsia. Prepartum serum and postpartum placental tissue samples were collected. Serum and placenta MFG-E8 and SOCS-3 levels were analysed with enzyme-linked immuno sorbent assay method. Results:In preeclamptic group, serum MFG-E8 levels raised and showed statistically significant difference with respect to control group (p<0.01). Placental SOCS-3 levels were significantly high in preeclamptic group compared to that in control group. Serum MFG-E8 levels showed positive correlation with both of blood pressure and proteinuria level. Conclusions:In our study, serum MFG-E8 level showed close relation with blood pressure and proteinuria. Increased placental SOCS-3 levels might be the result of compensatory angiogenic and anti-inflammatory response in PE. New studies with expanded populations and genetic evaluations are needed to discuss our results.

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Plasma IL-17, IL-35, interferon-γ, SOCS3 and TGF-β levels in pregnant women with preeclampsia, and their relation with severity of disease

Abstract: Increased IFN-gamma/TGF-beta production and reduced IL-35/IL-17/SOCS3 production in preeclamptic women may lead to less cytokine inhibitory activity in PE, which may account for the increased proteinuria and blood pressure in PE.

Cited by 53 publications

References 29 publications

Increased circulating interleukin-17 levels in preeclampsia

Increased circulating interleukin-17 levels in preeclampsia

A Dormant Microbial Component in the Development of Preeclampsia

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