Cytokine release from adipose tissue of nonobese individuals

Sopasakis, Victoria Rotter; Nagaev, Ivan; Smith, Ulf

doi:10.1038/sj.ijo.0803002

Cited by 45 publications

(33 citation statements)

References 21 publications

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“…Other proteins such as IL-1b, ICAM-1, MIF, MIP1a, MIP1b, and VEGF were not detected when adipocytes were incubated with control media. Although TNF-a was reported to be expressed in adipocytes [Sopasakis et al, 2005], its secretion was also undetectable in our cultures. In fact, other authors have demonstrated that TNF-a protein release from human adipose tissue was mainly due to non-fat cells [Fain et al, 2004b].…”

Section: Discussioncontrasting

confidence: 50%

Study of the proinflammatory role of human differentiated omental adipocytes

Bassols

Ortega

Moreno-Navarrete

et al. 2009

J of Cellular Biochemistry

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Infiltration of monocyte-derived macrophages into adipose tissue has been associated with tissue and systemic inflammation. It has been suggested that macrophage infiltration affects fat expansion through a paracrine action on adipocyte differentiation. Our working hypothesis is that factors released by monocytes/macrophages may also affect mature adipocyte biology. Human differentiated omental adipocytes were incubated with LPS and conditioned media obtained from human macrophage-like cell line THP-1, previously activated or not with LPS. We show that LPS greatly increased the secretion levels of pro-inflammatory adipokines including IL-6, IL-8, GRO, and MCP-1. Macrophage-conditioned medium also upregulated IL-6, IL-8, GRO, and MCP-1 mRNA expression and protein levels and led to the novo secretion of ICAM-1, IL-1 beta, IP-10, MIP-1 alpha, MIP-1 beta, VEGF, and TNFalpha. Human differentiated adipocytes treated by macrophage-conditioned medium displayed marked reduction of adipocyte function as assessed by decreased phosphorylation levels of ERK1, ERK2, and p38 alpha and reduced gene expression of lipogenic markers including PPAR-gamma and fatty acid synthase. These data show that macrophage-secreted factors not only inhibit the formation of mature adipocytes but alter their function, suggesting that human differentiated omental adipocytes might also contribute to systemic chronic low-grade inflammation associated with human obesity.

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Section: Discussioncontrasting

confidence: 50%

Study of the proinflammatory role of human differentiated omental adipocytes

Bassols

Ortega

Moreno-Navarrete

et al. 2009

J of Cellular Biochemistry

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“…In contrast, as for the regulation of adiponectin levels, several studies have reported a role of TNF-α [29][30][31], which quite likely induces the production of IL-6 [32]. TNF-α has been shown to reduce the gene expression and secretion of adiponectin from preadipocytes [30] as well as adipose tissue [31].…”

Section: Discussionmentioning

confidence: 88%

Contribution of adipocytokines to low-grade inflammatory state as expressed by circulating C-reactive protein in Japanese men: Comparison of leptin and adiponectin

Sugiura

Koji

Yatsuya

et al. 2008

International Journal of Cardiology

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“…Obesity is considered a chronic immune-inflammatory disease that causes incurable adult health problems such as type II diabetes, cardiovascular disorders and cancer [1][2][3][4][5] . Several animal models have been used to study obesity and related disorders; these include mice with leptin (ob/ob) or leptin receptor (db/db) mutation.…”

Section: Discussionmentioning

confidence: 99%

“…The infiltration of macrophages into the adipose tissue observed in the obese state worsens the inflammatory situation of white fat 3 . Plasma-circulating adipokines and pro-inflammatory cytokines that are secreted from the cells with monocyte/macrophage phenotype may represent a mechanism for several obese-related adult health problems like type II diabetes [3][4][5]9 . Along with a clear association between immune-inflammatory responses and obesity, systemic cellular immune modulatory responses other than inflammation in obese targets have been also reported.…”

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confidence: 99%

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Systemic immunity of obese-diabetes model (db/db) mice

Lee

Jang

Park

et al. 2010

Mol. Cell. Toxicol.

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Obesity has recently been defined as a chronic inflammatory disease and is considered as a major cause of adult health problems including incurable diseases like diabetes and cancer. In this study, the systemic immunity, including the innate and adaptive immunity parameters, of naturally occurring (leptin receptor mutation) obesity-diabetes mice (db/db) was examined to increase our knowledge of these mice for obesity-related studies. Severe fatty liver with blood engorgement was observed in the db/db mice. Compared to background C57BL/6J mice, the adaptive immunity, as measured by mitogen-induced T and B cell proliferation and cytokine release, was significantly suppressed in db/db mice. However, significant upregulation of innate immune-inflammatory parameters including macrophage function and NK cell activity was observed in db/db mice without external stimulation. These data conclusively confirm the systemic immune-inflammatory micro-environment with suppressed adaptive immunity of db/db mice, which may cause the secondary obesity-related life-threatening diseases like diabetes or cancer.Keywords Obese-diabetes model, Systemic immunity, db/db mice In modern society, obesity is considered a disease that causes incurable adult health problems including type II diabetes, cardiovascular disorders and cancer 1-5 . Recent findings indicate that obesity is a chronic inflammatory disease 3,6,7 . Increased NF-κB nuclear binding is known to be related with inflammation in obesity 3 . Inflammation-related molecules like adiponectin, cytokines (TNF-α, IL-1β or IL-6) and chemokines are secreted from white adipocytes and macrophages. The infiltration of macrophages into the adipose tissue observed in the obese state worsens the inflammatory situation of white fat 3 . Plasma-circulating adipokines and pro-inflammatory cytokines that are secreted from the cells with monocyte/macrophage phenotype may represent a mechanism for several obese-related adult health problems like type II diabetes [3][4][5]9 . Along with a clear association between immune-inflammatory responses and obesity, systemic cellular immune modulatory responses other than inflammation in obese targets have been also reported. Obesity-related systemic immune responses such as cytokine dysregulation and lipotoxicity can cause insulin resistance and metabolic disease, which increase the lethality in patients through internal organ destruction or infection 9,10 . Evidences from human as well as animal model suggest that obesity may be associated with immunodeficiency state including significantly impaired T cell responses 5-8 . Interestingly, modulation of regulatory T cell responses confirmed by increased transcription factor FoxP 3 in the lymphocytes was observed in leptin-deficient obese (ob/ob) mice 2 . In this study, the systemic immunity, including the innate and adaptive immune parameters, of naturally occurring obese-diabetic mice (db/db; leptin receptor mutation) was examined to increase our basic knowledge for obesity-related studies. Leptin is adipocyt...

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Cytokine release from adipose tissue of nonobese individuals

Cited by 45 publications

References 21 publications

Study of the proinflammatory role of human differentiated omental adipocytes

Study of the proinflammatory role of human differentiated omental adipocytes

Contribution of adipocytokines to low-grade inflammatory state as expressed by circulating C-reactive protein in Japanese men: Comparison of leptin and adiponectin

Systemic immunity of obese-diabetes model (db/db) mice

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