Inflammatory Gene Expression in Neck Perivascular and Subcutaneous Adipose Tissue in Men With Carotid Stenosis

Angiology ◽  
2021 ◽  
pp. 000331972110125
Author(s):  
Vlatka Pandzic Jaksic ◽  
Danijela Grizelj ◽  
Ana Livun ◽  
Marko Ajduk ◽  
Drago Boscic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Carotid Stenosis ◽  
Carotid Atherosclerosis ◽  
Study Groups ◽  
Control Group ◽  
Tissue Samples ◽  
Inflammatory Gene Expression ◽  
Monocyte Chemoattractant Protein 1 ◽  
Inflammatory Gene

The inflammatory phenotype of neck adipose tissue (NAT) might reflect its involvement in the pathogenesis of carotid atherosclerosis. We investigated inflammatory gene expression in the subcutaneous and the perivascular (pericarotid) adipose tissue from patients with carotid stenosis (CS) undergoing endarterectomy and a control group of patients without significant carotid atherosclerosis undergoing thyroid surgery. Only male patients were included (n = 13 in each study group). Clinical and biochemical data along with serum leptin, adiponectin, and monocyte chemoattractant protein 1 (MCP-1) were collected. Adipose tissue samples were obtained from both the subcutaneous and pericarotid compartments. Real-time polymerase chain reaction was used to measure gene expression of macrophage markers and adipokines. The CS group had higher subcutaneous and pericarotid visfatin gene expression and higher pericarotid expression of MCP-1 and CD68 genes. The ratio between pericarotid CD206 and CD68 gene expression was similar between study groups. Adiponectin gene expression in both NAT compartments did not differ between groups, but it was negatively associated with body weight. These observations suggest that NAT, and especially the pericarotid compartment, express enhanced inflammatory properties in patients with CS, but the proportion of anti-inflammatory macrophages in advanced atherosclerosis seems to be maintained.

Pro-inflammatory gene expression in adipose tissue in patients with atherosclerosis

2016 ◽  
Vol 252 ◽  
pp. e174 ◽  
Author(s):  
S. Čejková ◽  
I. Králová Lesná ◽  
J. Froněk ◽  
A. Králová ◽  
R. Poledne
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Inflammation, but not recruitment, of adipose tissue macrophages requires signalling through Mac-1 (CD11b/CD18) in diet-induced obesity (DIO)

2017 ◽  
Vol 117 (02) ◽  
pp. 325-338 ◽  
Author(s):  
Dennis Wolf ◽  
Nora Bukosza ◽  
David Engel ◽  
Marjorie Poggi ◽  
Felix Jehle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Inflammatory Gene Expression ◽  
Tissue Inflammation ◽  
Inflammatory Gene ◽  
Diet Induced Obesity ◽  
Adipose Tissue Macrophages ◽  
Cell Accumulation

SummaryCell accumulation is a prerequisite for adipose tissue inflammation. The leukocyte integrin Mac-1 (CD11b/CD18, αMβ2) is a classic adhesion receptor critically regulating inflammatory cell recruitment. Here, we tested the hypothesis that a genetic deficiency and a therapeutic modulation of Mac-1 regulate adipose tissue inflammation in a mouse model of diet-induced obesity (DIO). C57Bl6/J mice genetically deficient (Mac-1-/-) or competent for Mac-1 (WT) consumed a high fat diet for 20 weeks. Surprisingly, Mac-1-/- mice presented with increased diet-induced weight gain, decreased insulin sensitivity in skeletal muscle and in the liver in insulin-clamps, insulin secretion deficiency and elevated glucose levels in fasting animals, and dyslipidaemia. Unexpectedly, accumulation of adipose tissue macrophages (ATMs) was unaffected, while gene expression indicated less inflamed adipose tissue and macrophages in Mac-1-/- mice. In contrast, inflammatory gene expression at distant locations, such as in skeletal muscle, was not changed. Treatment of ATMs with an agonistic anti-Mac-1 antibody, M1/70, induced pro-inflammatory genes in cell culture. In vivo, treatment with M1/70 induced a hyper-inflammatory phenotype with increased expression of IL-6 and MCP-1, whereas accumulation of ATMs did not change. Finally, inhibition of Mac-1’s adhesive interaction to CD40L by the peptide inhibitor cM7 did not affect myeloid cell accumulation in adipose tissue. We present the surprising finding that adhesive properties of the leukocyte integrin Mac-1 are not required for macrophage accumulation in adipose tissue. Instead, Mac-1 modulates inflammatory gene expression in macrophages. These findings question the net effect of integrin blockade in cardio-metabolic disease.D. W., N. B., and D. E. equally contributed to this work.K. P., E. L., and A. Z. share senior authorship.Note: The review process for this manuscript was fully handled by Gregory Y. H. Lip, Editor in Chief.Supplementary Material to this article is available online at www.thrombosis-online.com.

scholarly journals Increased asthma and adipose tissue inflammatory gene expression with obesity and Inuit migration to a western country

2016 ◽  
Vol 111 ◽  
pp. 8-15 ◽  
Author(s):  
Vibeke Backer ◽  
Katherine J. Baines ◽  
Heather Powell ◽  
Celeste Porsbjerg ◽  
Peter G. Gibson
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Western Country ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

scholarly journals P050 Effect of biological treatments (anti-TNFs) in the creeping fat of Crohn’s disease patients

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S158-S159
Author(s):  
D Montfort-Ferré ◽  
C Serena ◽  
M Millan ◽  
A Boronat-Toscano ◽  
E Maymó-Masip ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Low Grade ◽  
Inflammatory Gene Expression ◽  
Histological Studies ◽  
Inflammatory Gene ◽  
Inflammatory Status ◽  
Mesenteric Fat

Abstract Background Crohn’s disease (CD) is characterized by persistent inflammation and ulcerations at the small or large bowel, provoking chronic low-grade systemic inflammation. Adipose tissue (AT) is believed to play an active role in the pathogenesis of CD, as the expansion of mesenteric fat attached to the inflamed segments of the intestine, also known as “creeping fat,” is a hallmark of the disease that seems to be directly related to disease activity. We demonstrated that adipose-stem cells (ASC) isolated from the creeping fat of CD patients showed a proinflammatory phenotype and increased the proliferation, migration, and phagocytic capacities of these cells. Taking into account the widely described effects of TNFalpha on the biology and functionality of adipocytes, we believe that biological therapies based on anti-TNF agents modify the inflammatory status of creeping fat. In this context, the effect of anti-TNF treatment on mesenteric fat is poorly studied, and the results are divergent. Methods Creeping fat biopsies were obtained from active CD patients that underwent surgery for symptomatic complications: 10 patients were on anti-TNF therapy (at least 6-months prior to surgery) and 10 patients never received any biological therapy. The groups were comparable in age, sex, and body mass index. We isolated from AT biopsies: AT explants, ASC, and adipose tissue macrophages (ATM). Adipose tissue was fixed in 10% phosphate-buffered formalin and embedded in paraffin for histological studies. The proliferation of ASC was performed using the CellTraceTM Violet Cell proliferation kit using flow cytometry and the cell migration of ASC was analyzed using a Tranwell system (8 mmpore polycarbonate membrane). Results Histological studies revealed that AT of patients treated with anti-TNF therapy recovered adipocytes morphology and showed lower infiltration of immune cells. Interestingly, we found a significant decrease in the gene expression of pro-inflammatory cytokines (IL1B, IL6, TNFA) in the creeping fat of CD patients treated with anti-TNF (Figure 1A). Furthermore, ATMs isolated from patients treated with anti-TNF showed a significant decrease in the gene expression of antigen-presenting markers (CD74, CIITa, HLA-DPB and HLA-DM) (Figure 1B). To note, ASC isolated from patients with anti-TNF therapy has significantly decreased their proliferation and migration capacities as well as the pro-inflammatory gene expression. Moreover, the anti-inflammatory gene expression and secretion were significantly increased in these cells (Figure 1C). Conclusion Anti-TNF therapies impact on the creeping fat of CD patients improving the phenotype of this tissue and this may cause a beneficial effect on CD.

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