Obesity and SARS-CoV-2 Infection a Multifaceted Interplay - Adipose Tissue Inflammation, Adipokine Disbalance and Immunity

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Cherneva RV ◽  
◽  
Valev D ◽  
Cherneva ZV ◽  
◽  
...  
Keyword(s):  
Adipose Tissue ◽  
T Cell ◽  
Viral Infections ◽  
Cell Number ◽  
Overweight And Obesity ◽  
Inflammasome Activation ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Insulin Resistant ◽  
And Function

Overweight and obesity are the most common comorbidities in SARSCoV- 2 patients, requiring hospitalization in intensive care units. The multifaceted nature of obesity including its effects on respiratory mechanics and immunity can fundamentally alter the pathogenesis of acute respiratory distress syndrome and pneumonia, which are the major causes of death due to SARS-CoV-2 infection. Most coronaviruses overcome host antiviral defense, and the pathogenicity of the virus is related to its capacity to suppress host immunity. Hyperleptinemia, insulin resistance and adipose tissue inflammation are hallmarks of obesity, which is associated with a leptin and insulin resistant state. Leptin regulates appetite and metabolism and through the Jak/STAT and Akt pathways modulates T cell number and function; insulin receptor signaling is closely engaged in T cell proliferation, whereas low garde adipose tissue inflammation provokes aberrant inflammasome activation. The review discusses these phenomena. It presents the reasons for susceptibility to respiratory viral infections in obese patients, as well as, the immunomodulatory effects of obesity to the outcome.

Alterations of the classic pathway of complement in adipose tissue of obesity and insulin resistance

2007 ◽  
Vol 292 (5) ◽  
pp. E1433-E1440 ◽  
Author(s):  
Jinhui Zhang ◽  
Wendy Wright ◽  
David A. Bernlohr ◽  
Samuel W. Cushman ◽  
Xiaoli Chen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Insulin Resistant ◽  
Obese Rats ◽  
Initial Activation ◽  
Adipose Cells ◽  
Classic Pathway

Adipose tissue inflammation has recently been linked to the pathogenesis of obesity and insulin resistance. C1 complex comprising three distinct proteins, C1q, C1r, and C1s, involves the key initial activation of the classic pathway of complement and plays an important role in the initiation of inflammatory process. In this study, we investigated adipose expression and regulation of C1 complement subcomponents and C1 activation regulator decorin in obesity and insulin resistance. Expression of C1q in epididymal adipose tissue was increased consistently in ob/ob mice, Zucker obese rats, and high fat-diet-induced obese (HF-DIO) mice. Decorin was found to increase in expression in Zucker obese rats and HF-DIO mice but decrease in ob/ob mice. After TZD administration, C1q and decorin expression was reversed in Zucker obese rats and HF-DIO mice. Increased expression of C1 complement and decorin was observed in both primary adipose and stromal vascular cells isolated from Zucker obese rats. Upregulation of C1r and C1s expression was also perceived in adipose cells from insulin-resistant humans. Furthermore, expression of C1 complement and decorin is dysregulated in TNF-α-induced insulin resistance in 3T3-L1 adipocytes and cultured rat adipose cells as they become insulin resistant after 24-h culture. These data suggests that both adipose and immune cells are the sources for abnormal adipose tissue production of C1 complement and decorin in obesity. Our findings also demonstrate that excessive activation of the classic pathway of complement commonly occurs in obesity, suggesting its possible role in adipose tissue inflammation and insulin resistance.

scholarly journals Obesity/insulin resistance rather than liver fat increases coagulation factor activities and expression in humans

2017 ◽  
Vol 117 (02) ◽  
pp. 286-294 ◽  
Author(s):  
Susanna Lallukka ◽  
Panu K. Luukkonen ◽  
You Zhou ◽  
Elina Isokuortti ◽  
Marja Leivonen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Coagulation Factor ◽  
Coagulation Factors ◽  
Liver Fat ◽  
Adipose Tissue Inflammation ◽  
Inflammatory Genes ◽  
Tissue Inflammation ◽  
Hepatic Expression ◽  
Insulin Resistant

SummaryIncreased liver fat may be caused by insulin resistance and adipose tissue inflammation or by the common I148M variant in PNPLA3 at rs738409, which lacks both of these features. We hypothesised that obesity/insulin resistance rather than liver fat increases circulating coagulation factor activities. We measured plasma prothrombin time (PT, Owren method), activated partial thromboplastin time (APTT), activities of several coagulation factors, VWF:RCo and fibrinogen, and D-dimer concentration in 92 subjects divided into groups based on insulin sensitivity [insulin-resistant (‘IR’) versus insulin-sensitive (‘IS’)] and PNPLA3 genotype (PNPLA3148MM/MI vs PNPLA3148II). Liver fat content (1H-MRS) was similarly increased in ‘IR’ (13 ± 1 %) and PNPLA3148MM/MI (12 ± 2 %) as compared to ‘IS’ (6 ± 1 %, p < 0.05) and PNPLA3148II (8 ± 1 %, p < 0.05), respectively. FVIII, FIX, FXIII, fibrinogen and VWF:RCo activities were increased, and PT and APTT shortened in ‘IR’ versus ‘IS’, in contrast to these factors being similar between PNPLA3148MM/MI and PNPLA3148II groups. In subjects undergoing a liver biopsy and entirely lacking the I148M variant, insulin-resistant subjects had higher hepatic expression of F8, F9 and FGG than equally obese insulin-sensitive subjects. Expression of pro-inflammatory genes in adipose tissue correlated positively with PT (% of normal), circulating FVIII, FIX, FXI, VWR:RCo and fibrinogen, and expression of anti-inflammatory genes negatively with PT (%), FIX and fibrinogen. We conclude that obesity/insulin resistance rather than an increase in liver fat is associated with a procoagulant plasma profile. This reflects adipose tissue inflammation and increased hepatic production of coagulation factors and their susceptibility for activation.Supplementary Material to this article is available online at www.thrombosis-online.com.

scholarly journals Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet-induced adipose tissue inflammation

2014 ◽  
Vol 96 (6) ◽  
pp. 1087-1100 ◽  
Author(s):  
Hiroe Honda ◽  
Yoshinori Nagai ◽  
Takayuki Matsunaga ◽  
Naoki Okamoto ◽  
Yasuharu Watanabe ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Nlrp3 Inflammasome ◽  
Potent Inhibitor ◽  
Inflammasome Activation ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Nlrp3 Inflammasome Activation

scholarly journals Pro-inflammatory effects of DEHP in SGBS-derived adipocytes and THP-1 macrophages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kristina Schaedlich ◽  
Laura-Sophie Beier ◽  
Judith Kolbe ◽  
Martin Wabitsch ◽  
Jana Ernst
Keyword(s):  
Adipose Tissue ◽  
Energy Homeostasis ◽  
Overweight And Obesity ◽  
Environmental Chemicals ◽  
Low Grade ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Secreted Factors ◽  
The Impact ◽  
Dehp Exposure

AbstractIn the member countries of the Organization for Economic Co-operation and Development (OECD), overweight and obesity affect the majority of the population. The use of environmental chemicals, such as the plasticizer DEHP, has largely increased simultaneously with this development. DEHP is an "obesogen" that interferes with normal adipocyte differentiation and energy homeostasis. Obesity in turn is accompanied by chronic low-grade adipose tissue inflammation, leading to metabolic disorders such as type II diabetes. The main actors in adipose tissue inflammation are adipocytes and macrophages. However, the impact of DEHP on adipose tissue inflammation and the crosstalk between adipocytes and macrophages are unknown and the subjects of the current study. The influence of DEHP on inflammation was investigated in human Simpson–Golabi–Behmel syndrome (SGBS)-derived adipocytes and human THP-1 macrophages. The proinflammatory markers IL8, MCP1, IL1β, TNFα and others were measured (qRT-PCR, ELISA) in SGBS-derived adipocytes treated with DEHP [day 0 (d0)–d4; 50 µg/ml] and THP-1 macrophages cultured with conditioned medium (CM) from DEHP-treated adipocytes (SGBS-CM) (from d4 and d8). DEHP exposure led to a proinflammatory state in SGBS-derived adipocytes (e.g., increased secretion of IL8 and MCP1). Surprisingly, exposure of THP-1 macrophages to SGBS-CM did not show DEHP-induced effects. However, we demonstrated that medium containing (pre)adipocyte-secreted factors had a significant impact on the expression and secretion of macrophage and inflammatory markers in THP-1 macrophages in general and led to the significantly increased accumulation of intracellular lipid droplets.

scholarly journals Adipokines as Drug Targets in Diabetes and Underlying Disturbances

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Vinícius Andrade-Oliveira ◽  
Niels O.S. Câmara ◽  
Pedro M. Moraes-Vieira
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Drug Targets ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Low Grade ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Therapeutic Implications ◽  
Insulin Resistant

Diabetes and obesity are worldwide health problems. White fat dynamically participates in hormonal and inflammatory regulation. White adipose tissue is recognized as a multifactorial organ that secretes several adipose-derived factors that have been collectively termed “adipokines.” Adipokines are pleiotropic molecules that gather factors such as leptin, adiponectin, visfatin, apelin, vaspin, hepcidin, RBP4, and inflammatory cytokines, including TNF and IL-1β, among others. Multiple roles in metabolic and inflammatory responses have been assigned to these molecules. Several adipokines contribute to the self-styled “low-grade inflammatory state” of obese and insulin-resistant subjects, inducing the accumulation of metabolic anomalies within these individuals, including autoimmune and inflammatory diseases. Thus, adipokines are an interesting drug target to treat autoimmune diseases, obesity, insulin resistance, and adipose tissue inflammation. The aim of this review is to present an overview of the roles of adipokines in different immune and nonimmune cells, which will contribute to diabetes as well as to adipose tissue inflammation and insulin resistance development. We describe how adipokines regulate inflammation in these diseases and their therapeutic implications. We also survey current attempts to exploit adipokines for clinical applications, which hold potential as novel approaches to drug development in several immune-mediated diseases.

scholarly journals Coinhibitory Suppression of T Cell Activation by CD40 Protects Against Obesity and Adipose Tissue Inflammation in Mice

Circulation ◽  
2014 ◽  
Vol 129 (23) ◽  
pp. 2414-2425 ◽  
Author(s):  
Dennis Wolf ◽  
Felix Jehle ◽  
Nathaly Anto Michel ◽  
Eva Nora Bukosza ◽  
Jennifer Rivera ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

scholarly journals Macrophage beta2-adrenergic receptor is dispensable for the adipose tissue inflammation and function

2021 ◽  
Vol 48 ◽  
pp. 101220
Author(s):  
Kasparas Petkevicius ◽  
Guillaume Bidault ◽  
Sam Virtue ◽  
Stephen A. Newland ◽  
Martin Dale ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adrenergic Receptor ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
And Function
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