Evidence map›Paper›PMID 39738492›Full record

ArticleInternational journal of obesity (2005)2025

Lack of fibro-inflammatory response in human mammary adipose tissue in obesity.

Frédérique Fallone, Marie Rebeaud, Caroline Bouche, Jessica Fontaine, Carlo Arellano, Manuelle Ducoux-Petit, Lucyle Orgerit, Rémi Deudon, Rémy Nicolle, Camille Franchet and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of obesity (2005), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

18 authors.

Frédérique FalloneInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France. frederique.fallone@ipbs.fr.ORCID 0000-0002-5723-8189
Marie RebeaudInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.ORCID 0009-0008-1093-8752
Caroline BoucheInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Jessica FontaineInstitut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université de Toulouse, INSERM, UPS, Toulouse, France.
Carlo ArellanoInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Manuelle Ducoux-PetitInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Lucyle OrgeritInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Rémi DeudonInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.ORCID 0000-0003-3028-8220
Rémy NicolleUniversité Paris Cité, Centre de Recherche sur l'Inflammation (CRI), INSERM, U1149, CNRS, ERL 8252, F-75018, Paris, France.
Camille FranchetDépartement d'Anatomo-Pathologie, Institut Universitaire du Cancer de Toulouse-Oncopole, Toulouse, France.
David EstèveInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Emmanuelle Mouton-BarbosaInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Stéphanie DauvillierInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Mohamed MoutahirInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Odile Burlet-SchiltzInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Anne Bouloumié *Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université de Toulouse, INSERM, UPS, Toulouse, France.
Charlotte Vaysse *Institut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Catherine Muller *Institut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France. muller@ipbs.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnderstanding how obesity impacts human mammary adipose tissue (MAT) biology is crucial for deciphering its role in mammary epithelium during both physiological and pathophysiological processes, including breast cancer. Hypertrophic mammary adipocytes and Crown-Like Structures are present in MAT of patients with obesity but whether these changes initiate a fibro-inflammatory response at the tissue level remains insufficiently explored.

objectiveWe investigated the markers of adipose tissue dysfunction (immune cell infiltration, secretion pattern and fibrosis) in tumor-free MAT of patients with obesity versus patients who are lean.

methodsTumor-free MAT were obtained from 96 women with (n = 43) or without (n = 53) obesity who underwent mastectomy for breast cancer risk reduction or treatment. Immune and non-immune cell infiltration were determined using flow cytometry. Bulk transcriptomic was used to characterize the phenotype of CD206+ macrophages whose infiltration is increased in patients with obesity. Conditioned-medium were prepared from MAT to characterize their secretome and dose adipokines and cytokines by ELISA assay. The extra-cellular matrix (ECM) deposition was evaluated by Masson trichrome staining on cross-stained sections, 3D imaging of red picrosirius-stained tissues and measure of hydroxyproline content.

resultsWe observed an increase of CD206+/HLA-DR+ macrophages in the stromal vascular fraction of MAT from patients with obesity compared to patients who are lean. Other immune cell infiltration and endothelial or adipose progenitor cell numbers were similar between groups. Bulk transcriptomics on CD206+ macrophages revealed a significant decrease in ECM component expression and processing in obesity. In addition, no heightened secretion of pro-inflammatory cytokines, TGF-β1 or MCP-1 was observed in the samples from patients with obesity. ECM characterization revealed an absence of fibrosis, with MAT of patients with obesity showing even a slightly reduced collagen secretion and deposition compared with their lean counterparts.

conclusionsObesity is not associated with inflammation nor fibrosis in MAT, highlighting its unique behavior.

Indexed as

Adipose TissueInflammationMammary Glands, HumanObesityAdultBreast NeoplasmsFemaleFibrosisHumansMiddle Aged

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.