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Monocytes from Pregnant Women with Pre-Eclampsia are Polarized to a M1 Phenotype
Problem This study evaluated whether the monocyte inflammatory state in pre‐eclampsia (PE) might be associated with polarization to either M1 classically or M2 alternatively activated monocyte subsets. Method of Study Eighty‐five women with (PE) and 52 normotensive (NT) pregnant women matched for ge...
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Published in: | American journal of reproductive immunology (1989) 2014-07, Vol.72 (1), p.5-13 |
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Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Problem
This study evaluated whether the monocyte inflammatory state in pre‐eclampsia (PE) might be associated with polarization to either M1 classically or M2 alternatively activated monocyte subsets.
Method of Study
Eighty‐five women with (PE) and 52 normotensive (NT) pregnant women matched for gestational age were included. Expression of surface receptors characteristic of M1, such as Toll‐like receptor (TLR)2, TLR4, and CD64, or M2, such as CD163 and CD206 monocyte subsets were evaluated in peripheral blood monocytes by flow cytometry. Tumour necrosis factor‐alpha (TNF‐α), interleukin‐(IL)‐12p40, IL‐12p70, and IL‐10 were evaluated in the supernatant of monocyte cultures by ELISA.
Results
Expression of TLR4 and CD64 by monocytes from pre‐eclamptic women was significantly higher, while the expression of CD163 and CD206 expression was significantly lower compared with NT pregnant women. Endogenous production of TNF‐α, IL‐12p40, and IL‐12p70 by monocytes was increased, while synthesis of IL‐10 was lower in women with PE than in NT pregnant women.
Conclusions
Monocytes from women with PE are classically activated, producing higher levels of pro‐inflammatory cytokines, and express surface receptors characteristic of the M1 subset. These results provide evidence that the systemic inflammatory environment in PE may differentiate and polarize these cells to the M1 phenotype. |
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ISSN: | 1046-7408 1600-0897 |
DOI: | 10.1111/aji.12222 |