Distribution of monocyte subsets and polarization in preeclampsia and intrauterine fetal growth restriction

Alahakoon, Thushari I.; Medbury, Heather; Williams, Helen; Fewings, Nicole; Wang, Xin M.; Lee, Vincent

doi:10.1111/jog.13770

Cited by 14 publications

(16 citation statements)

References 43 publications

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“…While Flt-1 weakly correlated with CD163, the findings are consistent with Flt-1 related M1 upregulation of macrophages demonstrated in preeclamptic decidua [40] and may reflect monocyte activity such as chemotaxis. The inflammatory intermediate monocyte subset has been shown to be increased in preterm preeclampsia and fetal growth restriction as well as term pregnancy [34]. The current study findings of a gestational increase in Flt-1 and endoglin as well as with M1 polarization may represent an increase in the Flt-1 and endoglin expression by more inflammatory monocytes.…”

Section: Discussionsupporting

confidence: 49%

“…CD86 is a cell surface protein strongly expressed by M1-type macrophages / monocytes [[31], [32], [33]]. The monocyte expression of anti-inflammatory molecule, CD163 and the CD86/CD163 ratio can be used as a marker of M1 and M2 phenotypes [34]. M2 polarized macrophages play a role in resolution of inflammation, accompanied by reduced pro-inflammatory cytokine secretion [35].…”

Section: Introductionmentioning

confidence: 99%

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Maternal Flt-1 and endoglin expression by circulating monocyte subtype and polarization in preeclampsia and fetal growth restriction

Alahakoon¹,

Medbury²,

Williams³

et al. 2019

European Journal of Obstetrics & Gynecology and Reproductiv

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Objective Circulating levels of the anti-angiogenic factors sFlt-1 and sEndoglin are elevated in preeclampsia (PE) and fetal growth restriction (FGR), mainly secreted from placental trophoblast. This study aims to identify the contributory role of monocyte Flt-1 and endoglin expression in PE and FGR. Study design A prospective cross-sectional study was conducted and patients recruited from four clinical groups including normal pregnancy, PE, FGR and PE + FGR. Peripheral blood samples and cord blood were collected from 54 pregnant women between 24–40 weeks of gestation. Monocyte subset distribution was assessed using CD14 and CD16 expression and the surface expression of Flt-1, endoglin, CD86 and CD163 assessed by flow cytometry. We compared these factors between (1) clinical groups. (2) monocyte subset (3) monocyte polarization and (4) gestational age. Results Across all clinical groups, Flt-1 was mainly expressed by classical and intermediate monocytes, but no differences between clinical groups were observed. Surface expression of endoglin was higher on intermediate and non-classical monocytes and decreased in PE + FGR total monocytes. Flt-1 and endoglin expression correlated with increasing gestational age as well as higher CD86/CD163 ratio favouring M1 polarisation. The fetal monocyte endoglin expression was increased in FGR. Conclusion We conclude that monocyte Flt-1 and endoglin expression increase with gestational age and with M1 polarization suggesting their upregulation with inflammatory changes in monocytes. Endoglin expression by M1 monocytes may play a part in increased cardiovascular risk associated with preeclampsia. Endoglin expression on fetal monocytes is increased in FGR as a likely response to placental injury.

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Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

Maternal Flt-1 and endoglin expression by circulating monocyte subtype and polarization in preeclampsia and fetal growth restriction

Alahakoon¹,

Medbury²,

Williams³

et al. 2019

European Journal of Obstetrics & Gynecology and Reproductiv

Self Cite

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show abstract

“…Recent investigations confirm the previous findings on its relevance. In recent work of Alahakoon and colleagues, the authors estimated quantities of classical, intermediate and non-classical monocytes in blood samples from preeclamptic patients (with or without intrauterine growth restriction, IUGR) and uncomplicated pregnancies [92]. The authors observed a significantly lower content of classical monocytes for both PE groups (with or without IUGR), while the number of inflammatory monocytes which combined intermediate and non-classical subsets for these groups was significantly increased as compared with the control.…”

Section: Monocyte–macrophage System During Pregnancymentioning

confidence: 99%

Role of the Monocyte–Macrophage System in Normal Pregnancy and Preeclampsia

Vishnyakova

Elchaninov

Fatkhudinov

et al. 2019

IJMS

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The proper functioning of the monocyte–macrophage system, an important unit of innate immunity, ensures the normal course of pregnancy. In this review, we present the current data on the origin of the monocyte–macrophage system and its functioning in the female reproductive system during the ovarian cycle, and over the course of both normal and complicated pregnancy. Preeclampsia is a crucial gestation disorder characterized by pronounced inflammation in the maternal body that affects the work of the monocyte–macrophage system. The effects of inflammation at preeclampsia manifest in changes in monocyte counts and their subset composition, and changes in placental macrophage counts and their polarization. Here we summarize the recent data on this issue for both the maternal organism and the fetus. The influence of estrogen on macrophages and their altered levels in preeclampsia are also discussed.

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“…Immunological dysfunction: There is clear evidence that the immune system in women with an IUGR pregnancy differs compared to those without IUGR (190). This study found that peripheral monocytes in women with an IUGR pregnancy had a more classically anti-inflammatory profile than monocytes from women with an uncompromised pregnancy.…”

Section: Overcoming the Hurdles To Progressmentioning

confidence: 99%

Knowledge Gaps and Emerging Research Areas in Intrauterine Growth Restriction-Associated Brain Injury

et al. 2019

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Intrauterine growth restriction (IUGR) is a complex global healthcare issue. Concerted research and clinical efforts have improved our knowledge of the neurodevelopmental sequelae of IUGR which has raised the profile of this complex problem. Nevertheless, there is still a lack of therapies to prevent the substantial rates of fetal demise or the constellation of permanent neurological deficits that arise from IUGR. The purpose of this article is to highlight the clinical and translational gaps in our knowledge that hamper our collective efforts to improve the neurological sequelae of IUGR. Also, we draw attention to cutting-edge tools and techniques that can provide novel insights into this disorder, and technologies that offer the potential for better drug design and delivery. We cover topics including: how we can improve our use of crib-side monitoring options, what we still need to know about inflammation in IUGR, the necessity for more human post-mortem studies, lessons from improved integrated histology-imaging analyses regarding the cell-specific nature of magnetic resonance imaging (MRI) signals, options to improve risk stratification with genomic analysis, and treatments mediated by nanoparticle delivery which are designed to modify specific cell functions.

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Distribution of monocyte subsets and polarization in preeclampsia and intrauterine fetal growth restriction

Abstract: These results show for the first time, a shift towards increased intermediate maternal monocyte subtype in IUGR and in preterm PE as well as skewing of maternal peripheral monocytes (all subsets) towards M2 phenotype in pregnancies complicated by IUGR.

Cited by 14 publications

References 43 publications

Maternal Flt-1 and endoglin expression by circulating monocyte subtype and polarization in preeclampsia and fetal growth restriction

Maternal Flt-1 and endoglin expression by circulating monocyte subtype and polarization in preeclampsia and fetal growth restriction

Role of the Monocyte–Macrophage System in Normal Pregnancy and Preeclampsia

Knowledge Gaps and Emerging Research Areas in Intrauterine Growth Restriction-Associated Brain Injury

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