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Obesity in Pregnancy Stimulates Macrophage Accumulation and Inflammation in the Placenta
Open accessAbstract
Obesity and pregnancy are associated with a combination of insulin resistance and inflammatory changes which exacerbate in combination. Based on the similarity between the inflammatory transcriptomes of adipose tissue and placenta, we hypothesized that the placenta develops exaggerated inflammation in response to obesity. The aim of this study was to characterize placental inflammatory mediators and macrophage accumulation in relation to peripheral inflammation in obesity. Placental macrophages and maternal peripheral blood mononuclear cells (PBMC) from 20 obese and 15 lean women were functionally and phenotypically characterized using immunohistochemistry, flow cytometry and expression for macrophage markers and inflammatory cytokines. The number of resident CD68+ and CD14+ cells was increased 2-3 fold in the placenta of obese as compared to lean women. The macrophage population was characterized by a marked phenotypic heterogeneity with complex subsets of CD14+, CD68+ and CD11b+ (mac-1) cells and by an increased expression of the pro-inflammatory cytokines IL-1, TNF-alpha, IL-6. Placental inflammation was associated with an activation of PBMC gene expression with an increase in the monocyte differentiation and maturation markers CD14 and CD68 in maternal but not fetal PBMC. The inflammatory changes were associated with higher plasma concentrations of C-reactive protein and IL-6 in obese compared to lean women. In conclusion, the chronic inflammation state of pre-gravid obesity is extending to in utero life with accumulation of a heterogeneous macrophage population and pro-inflammatory mediators in the placenta. The resulting inflammatory milieu in which the fetus develops may have critical consequences for short and long term programming of obesity.
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“Increased oxidative stress and inflammation markers have been found in the placenta of obese mothers, suggesting a decisive role of an abnormal intrauterine environment in modulating fetal programming [76,79].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [79]
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“Therefore, fetuses of obese mothers are exposed to an imbalance of cytokines, as well as nutrients that can negatively affect fetal programming, leading to adverse long-term effects in the offspring.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [79]
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“The negative effect of maternal obesity on offspring health might be mediated by an alteration in the inflammatory state and an increase in oxidative stress due to excess adipose tissue.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [79]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Pregnancy is normally an inflammatory state caused by the remodeling of immunological system to allow embryo implantation, growth and life, regulated by a delicate balance of pro-inflammatory and anti-inflammatory cytokines; in pregnancies complicated by obesity, this balance is shifted mainly towards a pro-inflammatory state.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [79]
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“Evidence of a key role of inflammation in fetal programming was provided by Reynolds et al. in 2015, thanks to a study where supplementation with an anti-inflammatory molecule, the conjugated linoleic acid, led to a reduction in the expression of pro-inflammatory cytokines such as TNF-α and IL-1β and metabolic dysfunction in offspring [76,79].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [79]
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“A number of maternal conditions, both infectious and non-infectious, have been linked to placental inflammation (102, 453).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [102]
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Metadata
- Authors
- Challier, J. C., Basu, S., Bintein, T., Minium, J., Hotmire, K., Catalano, P. M., & Hauguel-de Mouzon, S.
- Affiliations
- Université Pierre-et-Marie-Curie (FR)
- MetroHealth (US)
- ORCID
- Catalano, P.M.
- Venue
- Placenta
- Publisher
- Elsevier BV
- Published
- 2008-03
- Volume
- 29
- Issue
- 3
- Pages
- 274-281
- ISSN
- 0143-4004 (ISSN-L)
- PMC
- PMC4284075
- OpenAlex
- W1975136933
- Cited by
- 712
- References
- 48
- Citations by year
- 2026: 18 · 2025: 32 · 2024: 25 · 2023: 47 · 2022: 57 · 2021: 30 · 2020: 66 · 2019: 33 · 2018: 44 · 2017: 48 · 2016: 51 · 2015: 67 · 2014: 53 · 2013: 46 · 2012: 34
- FWCI
- 22.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Placenta (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Deutsches Krebsforschungszentrum
- National Institutes of Health
- National Center for Research Resources (M01RR000080, RR 00080)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD022965, HD-22965)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- maternal obesity, placental inflammation, placental macrophages, macrophage heterogeneity, CD68, CD14, CD11b, inflammatory cytokines, interleukin-6, TNF-α, interleukin-1, C-reactive protein, insulin resistance, fetal programming
- MeSH terms
- CD68 Molecule, Adult, Calcium-Binding Proteins, Cell Count, Cells, Cultured, Female, Fetal Blood, Humans, Inflammation, Leukocytes, Mononuclear, Macrophages, Membrane Glycoproteins, Mucins, Obesity, Placenta, Pregnancy, Pregnancy Complications, Tumor Necrosis Factor-alpha, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Interleukin-6, Lipopolysaccharide Receptors, Receptors, G-Protein-Coupled
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