The imbalance of Th17/Treg axis involved in the pathogenesis of preeclampsia

Eghbal‐Fard, Shadi; Yousefi, Mehdi; Heydarlou, Hanieh; Ahmadi, Majid; Taghavi, Simin; Movasaghpour, Aliakbar; Jadidi‐Niaragh, Farhad; Yousefi, Bahman; Dolati, Sanam; Hojjat‐Farsangi, Mohammad; Rikhtegar, Reza; Nouri, Mohammad; Aghebati‐Maleki, Leili

doi:10.1002/jcp.27315

Cited by 103 publications

(86 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Excessive maternal inflammation, commonly involved in PE pathogenesis by an imbalance of Treg/Th17, is also a putative result of gut dysbiosis 26 47. In the current study, PE-FMT mice exhibited a mucosal and systematic imbalance of Treg and Th17 cells and exaggerated inflammation in the placenta.…”

Section: Discussionsupporting

confidence: 50%

See 1 more Smart Citation

Gut dysbiosis induces the development of pre-eclampsia through bacterial translocation

Chen

Liu

et al. 2020

Gut

206

180

View full text Add to dashboard Cite

ObjectivePre-eclampsia (PE) is one of the malignant metabolic diseases that complicate pregnancy. Gut dysbiosis has been identified for causing metabolic diseases, but the role of gut microbiome in the pathogenesis of PE remains unknown.DesignWe performed a case–control study to compare the faecal microbiome of PE and normotensive pregnant women by 16S ribosomal RNA (rRNA) sequencing. To address the causative relationship between gut dysbiosis and PE, we used faecal microbiota transplantation (FMT) in an antibiotic-treated mouse model. Finally, we determined the microbiome translocation and immune responses in human and mouse placental samples by 16S rRNA sequencing, quantitative PCR and in situ hybridisation.ResultsPatients with PE showed reduced bacterial diversity with obvious dysbiosis. Opportunistic pathogens, particularly Fusobacterium and Veillonella, were enriched, whereas beneficial bacteria, including Faecalibacterium and Akkermansia, were markedly depleted in the PE group. The abundances of these discriminative bacteria were correlated with blood pressure (BP), proteinuria, aminotransferase and creatinine levels. On successful colonisation, the gut microbiome from patients with PE triggered a dramatic, increased pregestational BP of recipient mice, which further increased after gestation. In addition, the PE-transplanted group showed increased proteinuria, embryonic resorption and lower fetal and placental weights. Their T regulatory/helper-17 balance in the small intestine and spleen was disturbed with more severe intestinal leakage. In the placenta of both patients with PE and PE-FMT mice, the total bacteria, Fusobacterium, and inflammatory cytokine levels were significantly increased.ConclusionsThis study suggests that the gut microbiome of patients with PE is dysbiotic and contributes to disease pathogenesis.

show abstract

Section: Discussionsupporting

confidence: 50%

“…Decreased regulatory T (Treg) cells and/or increased T helper-17 (Th17) cells play a central role in the pathogenesis of PE 26 27. Thus, we investigated whether the adverse effect observed with FMT was associated with changes in Treg/Th17 proportions.…”

Section: Resultsmentioning

confidence: 99%

Gut dysbiosis induces the development of pre-eclampsia through bacterial translocation

Chen

Liu

et al. 2020

Gut

206

180

View full text Add to dashboard Cite

show abstract

“…43 The dysregulation of this tight balance between Treg and Th17 cells has been shown to be involved in the pathogenesis of adverse pregnancy outcomes. 63 Indeed, decreased Treg cell numbers [65][66][67][68][69][70][71] and increased Th17 cell percentages 68,[72][73][74]…”

Section: Treg/ Th17 Cell Imbal An Ce and Adver S E Preg Nan C Y Outmentioning

confidence: 99%

COVID‐19 and Treg/Th17 imbalance: Potential relationship to pregnancy outcomes

Muyayalo

Huang

Zhao

et al. 2020

American J Rep Immunol

118

View full text Add to dashboard Cite

Coronavirus disease 2019 (COVID-19) is a pneumonia pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 1 First identified in December 2019 in an outbreak of pneumonia in Wuhan City (Hubei Province, China), COVID-19 currently affects over 210 countries and territories worldwide. 2 The World Health Organization (WHO) declared COVID-19 to be a Public Health Emergency of International Concern, 3 then a pandemic, on March 11, 2020. 4 By June 30, 2020, there had been over 10 million confirmed cases, including over 500.000 patient deaths. 2 The majority of COVID-19 patients manifest mild to moderate symptoms; approximately 15% progress to the severe form of the

show abstract

“…Compared with healthy pregnant women, a reduction in the expression of Treg-specific transcription factor Foxp3 and an elevation in Th17-specific transcription factor RORγt in patients with preeclampsia has been reported (178). Furthermore, analysis of cytokine profiles have revealed a significant decrease in IL-10, and a significant increase in IL-17 levels in patients with preeclampsia (178,179). Taken together, these studies suggest that a shift occurs from Tregs to Th17 cells in the development of preeclampsia, leading to an abnormal immune state that triggers inflammation and an impairment of immune tolerance.…”

Section: Preeclampsiamentioning

confidence: 99%

Role of Regulatory T Cells in Regulating Fetal-Maternal Immune Tolerance in Healthy Pregnancies and Reproductive Diseases

2020

View full text Add to dashboard Cite

Regulatory T cells (Tregs) are a specialized subset of T lymphocytes that function as suppressive immune cells and inhibit various elements of immune response in vitro and in vivo. While there are constraints on the number or function of Tregs which can be exploited to evoke an effective anti-tumor response, sufficient expansion of Tregs is essential for successful organ transplantation and for promoting tolerance of self and foreign antigens. The immune-suppressive property of Tregs equips this T lymphocyte subpopulation with a pivotal role in the establishment and maintenance of maternal tolerance to fetal alloantigens, which is necessary for successful pregnancy. Elevation in the level of pregnancy-related hormones including estrogen, progesterone and human chorionic gonadotropin promotes the recruitment and expansion of Tregs, directly implicating these cells in the regulation of fetal-maternal immune tolerance. Current studies have provided evidence that a defect in the number or function of Tregs contributes to the etiology of several reproductive diseases, such as recurrent spontaneous abortion, endometriosis, and pre-eclampsia. In this review, we provide insight into the underlying mechanism through which Tregs contribute to pregnancy-related immune tolerance and demonstrate the association between deficiencies in Tregs and the development of reproductive diseases.

show abstract

The imbalance of Th17/Treg axis involved in the pathogenesis of preeclampsia

Cited by 103 publications

References 46 publications

Gut dysbiosis induces the development of pre-eclampsia through bacterial translocation

Gut dysbiosis induces the development of pre-eclampsia through bacterial translocation

COVID‐19 and Treg/Th17 imbalance: Potential relationship to pregnancy outcomes

Role of Regulatory T Cells in Regulating Fetal-Maternal Immune Tolerance in Healthy Pregnancies and Reproductive Diseases

Contact Info

Product

Resources

About