Evidence map›Paper›PMID 28824621›Full record

ArticleFrontiers in immunology2017

Human Placental Hofbauer Cells Maintain an Anti-inflammatory M2 Phenotype despite the Presence of Gestational Diabetes Mellitus.

Carolin Schliefsteiner, Miriam Peinhaupt, Susanne Kopp, Jelena Lögl, Ingrid Lang-Olip, Ursula Hiden, Akos Heinemann, Gernot Desoye, Christian Wadsack

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

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  7. Hofbauer Cells in Pregnancies Complicated by Gestational Diabetes Mellitus and Pathological Fetal Growth.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
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7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Carolin SchliefsteinerPerinatal Research Laboratory, Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria.
Miriam PeinhauptDepartment of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Susanne KoppPerinatal Research Laboratory, Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria.
Jelena LöglPerinatal Research Laboratory, Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria.
Ingrid Lang-OlipDepartment of Cell Biology, Medical University of Graz, Graz, Austria.
Ursula HidenPerinatal Research Laboratory, Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria.
Akos HeinemannDepartment of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Gernot DesoyePerinatal Research Laboratory, Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria.
Christian WadsackPerinatal Research Laboratory, Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria.
Medical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHofbauer cells (HBCs) are macrophages of the feto-placental unit. Despite the general view that these cells have an anti-inflammatory M2 phenotype, recent studies have claimed that pregnancy pathologies-e.g., gestational diabetes mellitus (GDM)-cause a switch from an M2 to an M1 pro-inflammatory phenotype in HBCs. The pilot-study presented here challenges this claim, showing that HBCs maintain anti-inflammatory properties in spite of the hyperglycemic, low-grade inflammatory environment of GDM.

methodsHBCs were isolated from placentae of healthy women (

resultsFACS and immune staining showed that, indeed, M2 markers, such as CD206 and CD209, are increased in HBCs isolated from GDM placentae. Also, the M1 marker CD86 was increased, but only by trend. Secretion of numerous cytokines, chemokines and growth factors was not changed; pro-inflammatory interleukin (IL)-1β and IL-6 release form GDM HBC was increased but not significant. Exposure to GDM HBC supernatant did not induce cell adhesion molecules (VCAM-1, selectins, vascular endothelial-cadherin) in placental endothelial cells compared to supernatant from control HBCs, an induction of intracellular adhesion molecule 1 was observed however.

conclusionOur study-although performed in a small set of patients-shows that placental macrophages maintain their anti-inflammatory, tissue remodeling M2 phenotype even in pregnancies affected by gestational diabetes. This consistent phenotype might be important for propagation of maternal tolerance toward the fetus and for protection of the fetus from a low-grade inflammatory environment.

Indexed as

gestational diabetesHofbauer cellsinflammationmacrophage phenotype/polarizationplacenta

Identifiers

PMID28824621
PMCPMC5534476
OpenAlexW2741123422

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.