Abdominal adipose tissue cytokine gene expression: relationship to obesity and metabolic risk factors

2005 ◽  
Vol 288 (4) ◽  
pp. E741-E747 ◽  
Author(s):  
Tongjian You ◽  
Rongze Yang ◽  
Mary F. Lyles ◽  
Dawei Gong ◽  
Barbara J. Nicklas

Adipose tissue is a major source of inflammatory and thrombotic cytokines. This study investigated the relationship of abdominal subcutaneous adipose tissue cytokine gene expression to body composition, fat distribution, and metabolic risk during obesity. We determined body composition, abdominal fat distribution, plasma lipids, and abdominal subcutaneous fat gene expression of leptin, TNF-α, IL-6, PAI-1, and adiponectin in 20 obese, middle-aged women (BMI, 32.7 ± 0.8 kg/m2; age, 57 ± 1 yr). A subset of these women without diabetes ( n = 15) also underwent an OGTT. In all women, visceral fat volume was negatively related to leptin ( r = −0.46, P < 0.05) and tended to be negatively related to adiponectin ( r = −0.38, P = 0.09) gene expression. Among the nondiabetic women, fasting insulin ( r = 0.69, P < 0.01), 2-h insulin ( r = 0.56, P < 0.05), and HOMA index ( r = 0.59, P < 0.05) correlated positively with TNF-α gene expression; fasting insulin ( r = 0.54, P < 0.05) was positively related to, and 2-h insulin ( r = 0.49, P = 0.06) tended to be positively related to, IL-6 gene expression; and glucose area ( r = −0.56, P < 0.05) was negatively related to, and insulin area ( r = −0.49, P = 0.06) tended to be negatively related to, adiponectin gene expression. Also, adiponectin gene expression was significantly lower in women with vs. without the metabolic syndrome (adiponectin-β-actin ratio, 2.26 ± 0.46 vs. 3.31 ± 0.33, P < 0.05). We conclude that abdominal subcutaneous adipose tissue expression of inflammatory cytokines is a potential mechanism linking obesity with its metabolic comorbidities.

2011 ◽  
Vol 20 (5) ◽  
pp. e153-e156 ◽  
Author(s):  
Clara Bambace ◽  
Mariassunta Telesca ◽  
Elena Zoico ◽  
Anna Sepe ◽  
Debora Olioso ◽  
...  

2010 ◽  
Vol 298 (1) ◽  
pp. C171-C181 ◽  
Author(s):  
Zachary A. Cooper ◽  
Arundhati Ghosh ◽  
Aditi Gupta ◽  
Tapan Maity ◽  
Ivor J. Benjamin ◽  
...  

We previously showed that exposure to febrile-range temperatures (FRT, 39.5–40°C) reduces LPS-induced TNF-α expression, in part through the direct interaction of heat shock factor-1 (HSF1) with the TNF-α gene promoter. However, it is not known whether exposure to FRT also modifies more proximal LPS-induced signaling events. Using HSF1-null mice, we confirmed that HSF1 is required for FRT-induced repression of TNF-α in vitro by LPS-stimulated bone marrow-derived macrophages and in vivo in mice challenged intratracheally with LPS. Exposing LPS-stimulated RAW 264.7 mouse macrophages to FRT reduced TNF-α expression while increasing IL-1β expression despite the two genes sharing a common myeloid differentiation protein-88 (MyD88)-dependent pathway. Global activation of the three LPS-induced signaling intermediates that lead to cytokine gene expression, ERK and p38 MAPKs and NF-κB, was not affected by exposing RAW 264.7 cells to FRT as assessed by ERK and p38 phosphorylation and NF-κB in vitro DNA-binding activity and activation of a NF-κB-dependent synthetic promoter. However, chromatin immunoprecipitation (ChIP) analysis demonstrated that exposure to FRT reduced LPS-induced recruitment of NF-κB p65 to the TNF-α promoter while simultaneously increasing its recruitment to the IL-1β promoter. These data suggest that FRT exerts its effects on cytokine gene expression in a gene-specific manner through distal effects on promoter activation rather than proximal receptor activation and signal transduction.


Author(s):  
Timothy G. Ramsay ◽  
Margo J. Stoll ◽  
Le Ann Blomberg ◽  
Thomas J. Caperna

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 360-361
Author(s):  
Sharon A Norton ◽  
Amanda A Adams

Abstract Senior horses often exhibit chronic inflammation and decreased immune responses. Dietary Saccharomyces cerevisiae fermentation product (SCFP; Diamond V, Cedar Rapids, IA) has been shown to affect immune responses in several species. This study aimed to evaluate SCFP-mediated immune function in senior horses. Sixteen horses (24.8 ± 3.0 y; BW = 545.8 ± 61.9 kg) were allotted to two treatments: CON (n = 8; no SCFP supplementation) and SCFP top dressed onto a common concentrate for 56 d (21 g/d; n = 8). Body condition score (BCS), BW, whole blood cytokine (INF-ɣ, TNF-α, IL-1β, IL-6, IL-10, IL-4, IL-8, IL-13, IL-17) and COX-1 and COX-2 gene expression were measured at d 0, 42, 49 and 56. Horses were challenged with a monovalent influenza vaccine at d 42 (MIV; Fluvacc Innovator; Zoetis Animal Health, Parsippany, NJ). Pre-MIV (d 0–42) and post-MIV (d 42–56) responses were analyzed using general mixed model procedures. Pre-MIV, BW tended to increase (P = 0.09) over time. Expression of IL-10 tended to be lower for SCFP than CON (P = 0.09) and IL-13 expression decreased over time (P &lt; 0.05). Post-MIV, BCS linearly increased over time (P = 0.006) while TNF-α tended to increase at d 49 and return to d 42 levels by d 56 (P = 0.06). Both INF-ɣ and IL-10 expression were lower for SCFP vs CON (P &lt; 0.05). Gene expression of COX-2 tended to decrease (P = 0.06) at d 49 and return to the d 42 baseline by d 56. Gene expression of IL-13 tended to decrease with SCFP but increased with CON at d 49 with both returning to d 42 levels by d 56 (P = 0.08). Influenza H1 titers increased over time post-vaccination (P &lt; 0.001) with no difference between treatments. Dietary SCFP may modulate pro-inflammatory and anti-inflammatory cytokine gene expression in senior horses.


2000 ◽  
Vol 7 (5) ◽  
pp. 769-773 ◽  
Author(s):  
Elizabeth Crabb Breen ◽  
Matthew McDonald ◽  
Jiang Fan ◽  
John Boscardin ◽  
John L. Fahey

ABSTRACT Evaluation of cytokine gene expression following in vitro stimulation is one means of examining the dysregulation of the immune system in human immunodeficiency virus (HIV) infection. We have assessed differences in the immune status of non-HIV-infected (HIV−) and HIV-infected (HIV+) individuals by evaluating the kinetics of the expression of cytokine genes. We compared detailed time courses of cytokine mRNA expression in HIV− and HIV+ peripheral blood mononuclear cells (PBMC) and found that there is a significant shift (P < 0.01) for all cytokines examined (interleukin 2 [IL-2], IL-6, IL-10, gamma interferon, and tumor necrosis factor alpha [TNF-α]) to an earlier time of mean peak mRNA expression by HIV+ PBMC (between 4 and 8 h) compared to HIV− PBMC (8 h) in response to either phytohemagglutinin (PHA) or anti-CD3 stimulation. Additional studies showed that although PHA-stimulated HIV+ PBMC showed decreased median IL-2, IL-4, and TNF-α mRNA levels, they typically demonstrated more rapid kinetics (increased mean 4-h/24-h cytokine mRNA ratios), with significant differences for IL-4 (P < 0.05) and TNF-α (P < 0.005), compared to HIV− PBMC. The use of fresh or frozen cells gave comparable cytokine mRNA data; however, the secretion of some cytokine proteins (IL-2 receptor, IL-10, and TNF-α) appeared to be reduced in HIV+ PBMC that had been frozen and thawed. Our studies demonstrate that the kinetics of cytokine gene expression can reveal additional dysregulation of the immune system in HIV infection, suggesting that PBMC of HIV-infected persons exist in an activated state in vivo that permits them to express cytokine genes more rapidly than a normal PBMC.


2015 ◽  
Vol 308 (12) ◽  
pp. R1062-R1069 ◽  
Author(s):  
Jennifer E. Dumaine ◽  
Noah T. Ashley

Sleep deprivation induces acute inflammation and increased glucocorticosteroids in vertebrates, but effects from fragmented, or intermittent, sleep are poorly understood. Considering the latter is more representative of sleep apnea in humans, we investigated changes in proinflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokine gene expression in the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) of a murine model exposed to varying intensities of sleep fragmentation (SF). Additionally, serum corticosterone was assessed. Sleep was disrupted in male C57BL/6J mice using an automated sleep fragmentation chamber that moves a sweeping bar at specified intervals (Lafayette Industries). Mice were exposed to bar sweeps every 20 s (high sleep fragmentation, HSF), 120 s (low sleep fragmentation, LSF), or the bar remained stationary (control). Trunk blood and tissue samples were collected after 24 h of SF. We predicted that HSF mice would exhibit increased proinflammatory expression, decreased anti-inflammatory expression, and elevated stress hormones in relation to LSF and controls. SF significantly elevated IL-1β gene expression in adipose tissue, heart (HSF only), and hypothalamus (LSF only) relative to controls. SF did not increase TNF-α expression in any of the tissues measured. HSF increased TGF-β1 expression in the hypothalamus and hippocampus relative to other groups. Serum corticosterone concentration was significantly different among groups, with HSF mice exhibiting the highest, LSF intermediate, and controls with the lowest concentration. This indicates that 24 h of SF is a potent inducer of inflammation and stress hormones in the periphery, but leads to upregulation of anti-inflammatory cytokines in the brain.


2021 ◽  
Author(s):  
Ana Elena Espinosa De Ycaza ◽  
Esben Søndergaard ◽  
Maria Morgan-Bathke ◽  
Kelli Lytle ◽  
Danae A. Delivanis ◽  
...  

The role of adipose tissue (AT) inflammation on AT function in humans is unclear. We tested whether AT macrophage (ATM) content, cytokine gene expression and senescent cell burden (markers of AT inflammation) predict AT insulin resistance measured as the insulin concentration that suppresses lipolysis by 50% (IC<sub>50</sub>). We studied 86 volunteers with normal weight or obesity at baseline, and a subgroup of 25 volunteers with obesity before and after weight loss. There was a strong, positive relationship between IC<sub>50 </sub>and abdominal subcutaneous and femoral fat cell size (FCS). The positive, univariate relationships between IC<sub>50 </sub>and abdominal AT inflammatory markers: CD68, CD14, CD206 ATM/100 adipocytes, senescent cells, IL-6 and TNF-α mRNA were not significant after adjustment for FCS. A 10% weight loss significantly reduced IC<sub>50</sub>, however, there was no reduction in adipose ATM content, senescent cells or cytokine gene expression. Our study suggests that commonly used markers of AT inflammation are not causally linked to AT insulin resistance, whereas FCS is a strong predictor of AT insulin resistance with respect to lipolysis.


2015 ◽  
Vol 35 (5) ◽  
pp. 396-402 ◽  
Author(s):  
David G.G. Schwarz ◽  
Pricila A.G. Pietralonga ◽  
Marina C.C. Souza ◽  
Isabel A. Carvalho ◽  
Rosyane S. Cruzeiro ◽  
...  

AbstractMycobacterium avium subspecies paratuberculosis (MAP) can infect ruminants and remain subclinical for long periods within herds. The identification of organs that are more susceptible to infection and the evaluation of cytokine expression at the site of infection are important to understand the pathogenesis of MAP. In this study, the probability of detection of MAP-DNA and the expression of cytokines in organs of C57BL/6 mice infected intraperitoneally for 120 days were evaluated. Among the evaluated organs, the spleen (85%), colon (75%) and liver (60%) had the highest frequency of positivity. When compared these frequencies between organs, it has been found that the spleen had 1.54 times as likely to be positive in relation to the ileum, and 2.0 times more likely in relation to the Peyer's patches. In addition, at 60 days post-infection, the spleen and the liver were responsible for upregulation of IFN-γ , and the ileum by TNF-α and IL-4. The results indicate that the spleen is the best organ for evaluating an experimental infection by MAP, especially in the initial stages of the infection. Moreover, it showed that the spleen, liver and ileum have a direct role in the inflammatory response in experimental models.


Sign in / Sign up

Export Citation Format

Share Document