scholarly journals Effect of Prepartum Adiposity and Lipolysis on Gestational and Postnatal Adipose Tissue Inflammation and Immune Cell Infiltration

2017 ◽  
Vol 31 (S1) ◽  
Author(s):  
Clarissa Strieder‐Barboza ◽  
Jonas Souza ◽  
Adam L. Lock ◽  
G. Andres Contreras
Keyword(s):  
Adipose Tissue ◽  
Immune Cell ◽  
Cell Infiltration ◽  
Immune Cell Infiltration ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

scholarly journals B Lymphocytes and Adipose Tissue Inflammation

2020 ◽  
Vol 40 (5) ◽  
pp. 1110-1122 ◽  
Author(s):  
Prasad Srikakulapu ◽  
Coleen A. McNamara
Keyword(s):  
Adipose Tissue ◽  
B Cell ◽  
Immune Cells ◽  
Immune Cell ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Cell Type ◽  
Tissue Inflammation ◽  
B Cell Subsets

The immune system plays an important role in obesity-induced adipose tissue inflammation and the resultant metabolic dysfunction, which can lead to hypertension, dyslipidemia, and insulin resistance and their downstream sequelae of type 2 diabetes mellitus and cardiovascular disease. While macrophages are the most abundant immune cell type in adipose tissue, other immune cells are also present, such as B cells, which play important roles in regulating adipose tissue inflammation. This brief review will overview B-cell subsets, describe their localization in various adipose depots and summarize our knowledge about the function of these B-cell subsets in regulating adipose tissue inflammation, obesity-induced metabolic dysfunction and atherosclerosis.

scholarly journals Increased adipose tissue aromatase activity improves insulin sensitivity and reduces adipose tissue inflammation in male mice

2017 ◽  
Vol 313 (4) ◽  
pp. E450-E462 ◽  
Author(s):  
Claes Ohlsson ◽  
Ann Hammarstedt ◽  
Liesbeth Vandenput ◽  
Niina Saarinen ◽  
Henrik Ryberg ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Sex Steroids ◽  
Immune Cell ◽  
Local Effect ◽  
Aromatase Activity ◽  
Adipose Tissue Inflammation ◽  
Male Mice ◽  
Tissue Inflammation ◽  
Pparg Expression

Females are, in general, more insulin sensitive than males. To investigate whether this is a direct effect of sex-steroids (SS) in white adipose tissue (WAT), we developed a male mouse model overexpressing the aromatase enzyme, converting testosterone (T) to estradiol (E2), specifically in WAT (Ap2-arom mice). Adipose tissue E2 levels were increased while circulating SS levels were unaffected in male Ap2-arom mice. Importantly, male Ap2-arom mice were more insulin sensitive compared with WT mice and exhibited increased serum adiponectin levels and upregulated expression of Glut4 and Irs1 in WAT. The expression of markers of macrophages and immune cell infiltration was markedly decreased in WAT of male Ap2-arom mice. The adipogenesis was enhanced in male Ap2-arom mice, supported by elevated Pparg expression in WAT and enhanced differentiation of preadipocyte into mature adipocytes. In summary, increased adipose tissue aromatase activity reduces adipose tissue inflammation and improves insulin sensitivity in male mice. We propose that estrogen increases insulin sensitivity via a local effect in WAT on adiponectin expression, adipose tissue inflammation, and adipogenesis.

scholarly journals CD40L Deficiency Attenuates Diet-Induced Adipose Tissue Inflammation by Impairing Immune Cell Accumulation and Production of Pathogenic IgG-Antibodies

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e33026 ◽  
Author(s):  
Dennis Wolf ◽  
Felix Jehle ◽  
Alexandra Ortiz Rodriguez ◽  
Bianca Dufner ◽  
Natalie Hoppe ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Immune Cell ◽  
Adipose Tissue Inflammation ◽  
Igg Antibodies ◽  
Tissue Inflammation ◽  
Cell Accumulation

scholarly journals Inhibition of CXCR2 by Glucocorticoids in Adipose Tissue

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A51-A51
Author(s):  
Shripa Amatya ◽  
Hemangini Dhaibar ◽  
Maria Grazia Petrillo ◽  
John A Cidlowski ◽  
Diana Cruz Topete
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Inflammatory Response ◽  
Immune Cell ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
The United States ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

Abstract Obesity-induced chronic adipose tissue inflammation is a significant risk factor for metabolic and cardiovascular disease (CVD), which affects 30.3 million adults in the United States. Interaction of adipocytes with hormonal, metabolic and immune systems play an integral role in the underlying pathophysiological mechanisms that leads to development of obesity-related complications. Despite this association, the mechanisms that coordinate the inflammatory mediators in causing adipose tissue inflammation are not well understood. Glucocorticoids (GC) are well known for their potent anti-inflammatory actions; however, the mechanism by which GC coordinate the inflammatory response of adipocytes are unknown. From our genome-wide microarray data derived from adipocyte-specific glucocorticoid receptor (GR) knockout (AdipoGRKO) mice, we found that GR inactivation leads to a significant increase in pro-inflammatory gene in white adipose tissue (WAT). Additionally, WAT isolated from AdipoGRKO mice showed significant increase in immune cell infiltration, which correlates with our gene expression data. Among the top up-regulated genes, we found the C-X-C Motif Chemokine Receptor 2 (Cxcr2), which is a powerful mediator of chemotaxis to the sites of inflammation. Although studies have shown the presence of Cxcr2 in adipocytes and suggested the contribution of Cxcr2 signaling in adipocyte development, its role in integrating adipose tissue inflammatory response is unknown. This led us to hypothesize that GR is critical to repress Cxcr2 gene expression and its pro inflammatory effects in adipocytes. Our in vitro studies using 3T3-L1 cells derived adipocytes showed that treatment with the synthetic glucocorticoid, Dexamethasone (Dex) led to a significant repression of Cxcr2 mRNA and protein levels. Furthermore, these effects are mediated by GR acting directly to repress Cxcr2 gene expression. Systemic administration of corticosterone significantly altered Cxcr2 expression in adipose tissue compared to untreated mice further supporting our results. Together our findings suggest that administration of glucocorticoids could inhibit adipose tissue inflammation and alleviate the comorbidities that arise from inflamed adipose tissue.

scholarly journals SUN-586 CXCR2 Repression by Glucocorticoids in Adipose Tissue

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Shripa Amatya ◽  
Natalie G Carroll ◽  
Maria Grazia Petrillo ◽  
John A Cidlowski ◽  
Diana Cruz Topete
Keyword(s):  
Adipose Tissue ◽  
Immune Cell ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
The United States ◽  
Adipose Tissue Inflammation ◽  
Immune Functions ◽  
Tissue Inflammation

Abstract Obesity-induced type 2 diabetes (T2D) is a significant risk factor of cardiovascular disease (CVD), which affects 28.1 million adults in the United States. Adipose tissue chronic inflammation is one of the main factors that drive obesity-induced insulin resistance (IR) and T2D. Despite several studies that have shown a link between obesity, adipose tissue inflammation, and IR/T2D, the mechanisms underlying this association are not well understood. Synthetic glucocorticoids are widely used for their potent anti-inflammatory actions; however, their use is hampered due to off-target side effects. Glucocorticoids exert profound effects on adipose tissue, including the regulation of adipocyte metabolism and immune functions. However, whether their effects on adipose tissue are positive or negative it is still a controversial topic. Genome-wide microarray data obtained from adipocyte-specific glucocorticoid receptor (GR) knockout (AdipoGRKO) mice showed that lack of GR leads to a significant increase in the expression of pro-inflammatory genes in white adipose tissue (WAT). Moreover, WAT isolated from adipoGRKO mice demonstrated significant increase in immune cell infiltration, which correlates with our gene expression data. Among the most up-regulated genes, we found the C-X-C Motif Chemokine Receptor 2 (CXCR2), which is a critical mediator of chemotaxis to the sites of inflammation. Although studies have shown the presence of CXCR2 in adipocytes and suggested the contribution of CXCR2 signaling in adipocyte development, its role in obesity-driven adipose tissue inflammation is unknown. This led us to hypothesize that adipocyte specific administration of glucocorticoids can reduce obesity-induced adipocyte inflammation by inhibiting CXCR2 gene transcription and signaling. Our in vitro studies using 3T3-L1 cells derived adipocytes showed that treatment with the synthetic glucocorticoid, Dexamethasone (Dex) led to a significant repression of CXCR2 mRNA and protein levels. Correlating with these results, Dex treatment significantly inhibited macrophage migration to adipocytes in a mechanism dependent on GR activation and repression of CXCR2. Furthermore, these results were recapitulated in vivo. Together our findings suggest that local delivery of glucocorticoids to adipose tissue could ameliorate inflammation and reduce the risk of developing IR and T2D.

PS19 - 88. Mast cell deficient mice on a high fat diet have altered immune cell infiltration in their adipose tissue

2012 ◽  
Vol 10 (3) ◽  
pp. 162-162
Author(s):  
Lianne van Beek ◽  
Ilze Bot ◽  
Amanda Pronk ◽  
Ko Willems van Dijk ◽  
Frits Koning ◽  
...  
Keyword(s):  
Mast Cell ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Immune Cell ◽  
Cell Infiltration ◽  
Immune Cell Infiltration ◽  
High Fat ◽  
Deficient Mice

Flavonoids in adipose tissue inflammation and atherosclerosis: one arrow, two targets

2020 ◽  
Vol 134 (12) ◽  
pp. 1403-1432 ◽  
Author(s):  
Manal Muin Fardoun ◽  
Dina Maaliki ◽  
Nabil Halabi ◽  
Rabah Iratni ◽  
Alessandra Bitto ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fruits And Vegetables ◽  
Metabolic Diseases ◽  
Therapeutic Agents ◽  
Adipose Tissue Inflammation ◽  
Cellular Mechanisms ◽  
Tissue Inflammation ◽  
Cholesterol Levels ◽  
Naturally Occurring ◽  
Pro Inflammatory Cytokines

Abstract Flavonoids are polyphenolic compounds naturally occurring in fruits and vegetables, in addition to beverages such as tea and coffee. Flavonoids are emerging as potent therapeutic agents for cardiovascular as well as metabolic diseases. Several studies corroborated an inverse relationship between flavonoid consumption and cardiovascular disease (CVD) or adipose tissue inflammation (ATI). Flavonoids exert their anti-atherogenic effects by increasing nitric oxide (NO), reducing reactive oxygen species (ROS), and decreasing pro-inflammatory cytokines. In addition, flavonoids alleviate ATI by decreasing triglyceride and cholesterol levels, as well as by attenuating inflammatory mediators. Furthermore, flavonoids inhibit synthesis of fatty acids and promote their oxidation. In this review, we discuss the effect of the main classes of flavonoids, namely flavones, flavonols, flavanols, flavanones, anthocyanins, and isoflavones, on atherosclerosis and ATI. In addition, we dissect the underlying molecular and cellular mechanisms of action for these flavonoids. We conclude by supporting the potential benefit for flavonoids in the management or treatment of CVD; yet, we call for more robust clinical studies for safety and pharmacokinetic values.

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