Adipocyte, Adipose Tissue, and Infectious Disease

Desruisseaux, Mahalia S.; Nagajyothi,; Trujillo, María E.; Tanowitz, Herbert B.; Scherer, Philipp E.

doi:10.1128/iai.01455-06

Cited by 123 publications

(115 citation statements)

References 150 publications

(164 reference statements)

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“…35,36 Recently, Ad infections were considered to play a role in the development of obesity and are associated with plasma lipid abnormalities. 15,17,18,37,38 In the present study it is shown that a range of different viral and bacterial microorganisms are able to infect human adipocytes and induce an inflammatory response. The production of IL-6 by adipocytes increased in a dose-and infection-dependent manner.…”

Section: Discussionmentioning

confidence: 60%

“…[9][10][11][12][13][14] It has been shown before that adenoviruses (Ad) are able to infect adipocytes 15,16 and that this is possibly related to the development of obesity. 17,18 Data from studies in animals indicate a possible role for virus infections in the etiology of human obesity. [19][20][21] Moreover, Ad-36 is associated with increased body weight and paradoxically lower cholesterol and triglyceride levels in Ad-36 antibody-positive vs -negative subjects.…”

Section: Introductionmentioning

confidence: 99%

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Infection-induced inflammatory response of adipocytes in vitro

et al. 2008

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Background: Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Methods: Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Results: Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192 ± 22 pg ml À1 (uninfected) to 1030 ± 86 pg ml À1 , 838 ± 59 pg ml À1 and 1241 ± 191 pg ml À1 , respectively (all Po0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285 ± 26.8 ng ml À1 vs uninfected: 477 ± 71.2 ng ml À1 ; P ¼ 0.05) and pre-adipocytes (709±43.3 ng ml À1 vs uninfected: 1071±71.8 ng ml À1 ; Po0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF-a production. Conclusions: Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes.

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Section: Discussionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Infection-induced inflammatory response of adipocytes in vitro

et al. 2008

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“…Brasaemle et al (1997) were the first to determine the mRNA expression of ADFP in the lungs, liver, testes, spleen, brain, heart, skeletal muscle, and kidneys of rats. The main cell types in abdominal fat and subcutaneous fat are fat cells,intramuscular fat gradually deposited between muscle bundles as chicken muscle fiber matures (Desruisseaux et al, 2007). Therefore, ADFP gene in the muscle and adipose tissues is mainly expressed in adipocytes.…”

Section: Correlation Analysis Of Relative Expression Of Apob Adfp Anmentioning

confidence: 99%

Correlation Analysis of Relative Expression of Apob, Adfp and Fatp1 with Lipid Metabolism in Daweishan Mini Chickens

Decai

ZhiYong

Zhang

et al. 2017

Rev. Bras. Cienc. Avic.

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Quantitative RT-PCR was applied to measure the relative expression levels of the adipose differentiation-related protein (ADFP) gene, fatty acid transport protein 1 (FATP1) gene and apolipoprotein B (ApoB) gene in subcutaneous fat, abdominal fat, liver and muscle at five growth stages (28, 49, 70, 91 and 112 d) to determine the effect of the expression ofthese genes on fat deposition in Daweishan Mini chickens. The relative expression of ADFP gene mRNA in the abdominal fat andthe liver was significantly different between 49 d and 70 d (p<0.05). The relative ApoB gene expression on 91d was higher in the liver, followed by muscles,subcutaneous fat, and abdominal fat, and was significantly higher in the liver than in the other three tissues. FATP1 gene expression in the liver presented a significant positive correlation with subcutaneous fat thickness (p<0.05). The results of this study suggest that the three genes may control the fat development in Daweishan Mini chicken.

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“…Akan tetapi bagaimanakah perubahan kualitas dari adiposit pada jaringan adiposa setelah paparan patogen tersebut masih sangat minim diketahui. Di sisi lain, prevalensi penyakit infeksi di negara berkembang masih tinggi dan disebutkan terdapat hubungan antara infeksi dengan obesitas (Desruisseaux et al, 2007).…”

Section: Pendahuluanunclassified

Adiposopathy In Vitro Study The Effect of Toxoplasma Gondii Profilin Induction To The Expression of IL-6 and TNF-a as A Predictor Candidate of Adipocyte Dysfunction on Subcutan Adipocyte Culture

Sudjari

Susanto

Indra

2015

RJLS

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Metabolic syndrome is a group of several risk factors consist of hypertension, dyslipidemia, glucose intolerance disorder, obesity, and has a relationship with CVD pathomechanism. WHO was report in 2003 more than 300 million adult in the world suffered from obesity. The role of adipose tissue in infectious diseases and adipocyte quality changes after exposure to pathogen has not been revealed. On the other hand, the prevalence of infectious diseases in developing country is still high. Previous studies proved a relationship between infection of Toxoplasma gondii and tissue dysfunction. Profilin is a membrane component of Toxoplasma gondii that able to stimulate expression of proinflammation cytokines through TLR-11 upregulation, and predicted able to trigger the adipocyte dysfunction. The aim of this study is to knows the effect of profilin exposure in vitro on subcutaneous adipocyte to the expression of IL-6 and TNF-α. The measurement of IL-6 and TNF- levels was done by ELISA technique. The result showed profilin exposure doses 5, 15 and 25 ng / ml increasing IL-6. Profilin exposure cause adipocyte dysfunction through the increasing proinflammatory adipocytokine levels as pathomechanism of metabolic syndrome associated with adipose tissue.

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Adipocyte, Adipose Tissue, and Infectious Disease

Cited by 123 publications

References 150 publications

Infection-induced inflammatory response of adipocytes in vitro

Infection-induced inflammatory response of adipocytes in vitro

Correlation Analysis of Relative Expression of Apob, Adfp and Fatp1 with Lipid Metabolism in Daweishan Mini Chickens

Adiposopathy In Vitro Study The Effect of Toxoplasma Gondii Profilin Induction To The Expression of IL-6 and TNF-a as A Predictor Candidate of Adipocyte Dysfunction on Subcutan Adipocyte Culture

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