Impaired alternative macrophage differentiation of peripheral blood mononuclear cells from obese subjects.
Macrophage alternative differentiation and obesity
Title :
Impaired alternative macrophage differentiation of peripheral blood mononuclear cells from obese subjects.
Macrophage alternative differentiation and obesity
Macrophage alternative differentiation and obesity
Author(s) :
Bories, Gael [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Caiazzo, Robert [Auteur]
Service de chirurgie générale et endocrinienne
Thérapie cellulaire du diabète
Derudas, Bruno [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Copin, Corinne [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Raverdy, Violeta [Auteur]
Service de chirurgie générale et endocrinienne
Thérapie cellulaire du diabète
Pigeyre, Marie [Auteur]
Thérapie cellulaire du diabète
Pattou, Francois [Auteur]
Service de chirurgie générale et endocrinienne
Thérapie cellulaire du diabète
Staels, Bart [Auteur correspondant]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Chinetti-Gbaguidi, Giulia [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Caiazzo, Robert [Auteur]

Service de chirurgie générale et endocrinienne
Thérapie cellulaire du diabète
Derudas, Bruno [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Copin, Corinne [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Raverdy, Violeta [Auteur]
Service de chirurgie générale et endocrinienne
Thérapie cellulaire du diabète
Pigeyre, Marie [Auteur]

Thérapie cellulaire du diabète
Pattou, Francois [Auteur]
Service de chirurgie générale et endocrinienne
Thérapie cellulaire du diabète
Staels, Bart [Auteur correspondant]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Chinetti-Gbaguidi, Giulia [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Journal title :
Diabetes and Vascular Disease Research
Pages :
189-95
Publisher :
SAGE Publications
Publication date :
2012-07
ISSN :
1479-1641
English keyword(s) :
polarization
inflammation
gene expression
obesity
macrophages
inflammation
gene expression
obesity
macrophages
HAL domain(s) :
Sciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire
English abstract : [en]
Visceral obesity is a chronic, low-grade inflammatory disease that predisposes people to the metabolic syndrome, type 2 diabetes and its cardiovascular complications. Adipose tissue is not a passive storehouse for fat, but ...
Show more >Visceral obesity is a chronic, low-grade inflammatory disease that predisposes people to the metabolic syndrome, type 2 diabetes and its cardiovascular complications. Adipose tissue is not a passive storehouse for fat, but an endocrine organ synthesizing and releasing a variety of bioactive molecules, some of which are produced by infiltrated immune-inflammatory cells including macrophages. Two different subpopulations of macrophages have been identified in adipose tissue: pro-inflammatory 'classical' M1 and anti-inflammatory 'alternative' M2 macrophages, and their ratio is suggested to influence the metabolic complications of obesity. These macrophages derive primarily from peripheral blood mononuclear cells (PBMCs). We hypothesised that obesity and the metabolic syndrome modulate PBMC functions. Therefore, alteration of the monocyte response, and more specifically their ability to differentiate toward alternative anti-inflammatory macrophages, was assessed in PBMCs isolated from lean and obese subjects with or without alterations in glucose homeostasis. Our results indicate that PBMCs from obese subjects have an altered expression of M2 markers and that their monocytes are less susceptible to differentiate toward an alternative phenotype. Thus PBMCs in obesity are programmed, which may contribute to the inflammatory dysregulation and increased susceptibility to inflammatory diseases in these patients.Show less >
Show more >Visceral obesity is a chronic, low-grade inflammatory disease that predisposes people to the metabolic syndrome, type 2 diabetes and its cardiovascular complications. Adipose tissue is not a passive storehouse for fat, but an endocrine organ synthesizing and releasing a variety of bioactive molecules, some of which are produced by infiltrated immune-inflammatory cells including macrophages. Two different subpopulations of macrophages have been identified in adipose tissue: pro-inflammatory 'classical' M1 and anti-inflammatory 'alternative' M2 macrophages, and their ratio is suggested to influence the metabolic complications of obesity. These macrophages derive primarily from peripheral blood mononuclear cells (PBMCs). We hypothesised that obesity and the metabolic syndrome modulate PBMC functions. Therefore, alteration of the monocyte response, and more specifically their ability to differentiate toward alternative anti-inflammatory macrophages, was assessed in PBMCs isolated from lean and obese subjects with or without alterations in glucose homeostasis. Our results indicate that PBMCs from obese subjects have an altered expression of M2 markers and that their monocytes are less susceptible to differentiate toward an alternative phenotype. Thus PBMCs in obesity are programmed, which may contribute to the inflammatory dysregulation and increased susceptibility to inflammatory diseases in these patients.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
European Project :
Source :
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