Monocytes from Pregnant Women with Pre-Eclampsia are Polarized to a M1 Phenotype

Medeiros, Leonardo Teixeira Lopes de; Peraçoli, José Carlos; Bannwart-Castro, Camila F.; Romão, Mariana; Weel, Ingrid C.; Golim, Márjorie de Assis; Oliveira, Leandro G.; Kurokawa, Cilmery Suemi; Borges, Vera Therezinha Medeiros; Peraçoli, Maria Terezinha Serrão

doi:10.1111/aji.12222

Cited by 51 publications

(44 citation statements)

References 47 publications

(59 reference statements)

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“…Previous in vitro and in vivo experimental studies have indicated that IL-10 expression may influence preeclampsia pathogenesis (Medeiros et al, 2014;Cornelius et al, 2015;Wang et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in interleukin-6 and interleukin-10 may be associated with risk of preeclampsia

Fan

Wang

et al. 2017

Genet. Mol. Res.

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Section: Discussionmentioning

confidence: 99%

Polymorphisms in interleukin-6 and interleukin-10 may be associated with risk of preeclampsia

Fan

Wang

et al. 2017

Genet. Mol. Res.

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“…Preeclampsia (PE), characterized by hypertension and proteinuria after 20 weeks of gestation, is among the leading complications during pregnancy [1,2]. Importantly, the immune system has been revealed to be unbalanced in the maternal-fetal interface of PE subjects with the manifestation of elevated levels of proinflammatory cytokines, neutrophil activation and endothelial dysfunction [3,4].…”

Section: Introductionmentioning

confidence: 99%

MiR‐30a attenuates immunosuppressive functions of IL‐1β‐elicited mesenchymal stem cells via targeting TAB3

Ding

Miao

et al. 2015

FEBS Letters

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a b s t r a c tMesenchymal stem cells (MSCs) possess the ability to modulate the immune response, and their abnormalities are related to several diseases. We previously reported that miR-30a expression significantly increased in the maternal-fetal interface during preeclampsia (PE), but the effects of miR-30a on the immunoregulatory characteristics of MSCs are unclear. In this study, we determined that miR-30a over-expression inhibited the IL-1b-elicited activation of the nuclear factor jB (NF-jB) and JNK signaling pathways and the production of IL-6, cyclooxygenase 2 (COX2) and IL-8 by targeting transforming growth factor-b-activated kinase 1 binding protein 3 (TAB3) in MSCs. Moreover, the over-expression of miR-30a also impaired MSCs' anti-inflammatory effects on macrophages. These data demonstrated that miR-30a in MSCs may participate in the immune dysregulation of the maternal-fetal interface during PE.

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“…49 Medeiros and colleagues highlighted the fact that monocytes isolated from pre-eclamptic patients are stimulated and synthesized copious amounts of cytokines, for example, IL-12 and TNF-α, as well as high-affinity Fcɣ receptor and toll-like receptor 4 cell surface markers. 50 Thus, the above-mentioned observations related to the systemic inflammatory response in PE could evolve and polarize the immune cells in particular monocytes toward the M1 phenotype. 50 An interesting suggested model of PE etiology is the relation of viruses and bacteria to the stimulation of corresponding inflammasome by emphasizing danger.…”

Section: The Role Of Infl Ammati On In Pre-ecl Amps Iamentioning

confidence: 99%

“…50 Thus, the above-mentioned observations related to the systemic inflammatory response in PE could evolve and polarize the immune cells in particular monocytes toward the M1 phenotype. 50 An interesting suggested model of PE etiology is the relation of viruses and bacteria to the stimulation of corresponding inflammasome by emphasizing danger. To further expand on this, the excretion of IL-1β, IL-18, and IL-33 in the extracellular space may give rise to early stimulation of myometrial contractility.…”

Section: The Role Of Infl Ammati On In Pre-ecl Amps Iamentioning

confidence: 99%

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Inflammation—The role of ATP in pre‐eclampsia

2019

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Sterile inflammation may be initiated by molecules in the host organism that signal “damage” or “danger” also known as danger‐associated molecular pattern (DAMPs). In pre‐eclampsia (PE), a variety of DAMPs may be involved in the etiology or exacerbation of the disorder. Adenosine 5’‐triphosphate (ATP) is a key intracellular energy molecule as well as a ligand for purinergic receptors. In humans, under physiological conditions, extracellular ATP (eATP) levels are distinctly low, but can rise to several hundred fold when cells become injured, stressed, or even necrotic. This often initiates a sterile inflammatory response with eATP acting as a DAMP. Extracellular ATP and its derivative nucleotides synthetized by endonucleotidases exhibit many of their effects through purinergic receptors, via inflammatory cascades and the production of proinflammatory molecules. This is clearly seen in the P2X7 gated receptor, which is linked to release of cytokines of the interleukin‐1 family. Considering its fundamental role in innate immunity, an imbalance of P2X7 receptor activation may lead to deleterious effects in the coordination of placental vessel tone via the synthesis of various proinflammatory cytokines. This review explores the implication of DAMPs, specifically ATP and uric acid in the inflammation associated with PE.

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Monocytes from Pregnant Women with Pre-Eclampsia are Polarized to a M1 Phenotype

Cited by 51 publications

References 47 publications

Polymorphisms in interleukin-6 and interleukin-10 may be associated with risk of preeclampsia

Polymorphisms in interleukin-6 and interleukin-10 may be associated with risk of preeclampsia

MiR‐30a attenuates immunosuppressive functions of IL‐1β‐elicited mesenchymal stem cells via targeting TAB3

Inflammation—The role of ATP in pre‐eclampsia

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