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Table 2 Biomarkers related to obesity and their relevance in the inflammatory response

From: Intraoperative immunomodulatory effects of sevoflurane versus total intravenous anesthesia with propofol in bariatric surgery (the OBESITA trial): study protocol for a randomized controlled pilot trial

Biomarkers Relevance References
MMP-2 Ability to break down ECM. Potential role as activator or inhibitor in tissue remodeling, atherosclerosis, cardiovascular diseases, and obesity. Levels are increased in obesity [36,37,38]
MMP-9 Ability to break down ECM. Potential role as activator or inhibitor in tissue remodeling, cardiovascular diseases, and obesity. Levels are diminished in obesity [36]
CXCR2 Expressed on circulating neutrophils; critical for directing their migration to inflammatory sites [39]
IL-12 Associated with insulin resistance. Divergently regulated in relation to inflammatory stress, excessive energy intake, and genetic obesity [40]
CCL3 (MIP-1α) High transcript and protein levels in the white adipose tissue of the obese. Correlated with fasting plasma insulin concentrations in humans. Required for macrophage infiltration in adipose tissue with CCL2 [41,42,43,44]
CCL2 (MCP1) Required for macrophage infiltration of adipose tissue Adipose-tissue and serum CCL2 expression is increased through insulin stimuli, more in insulin-resistant than in insulin-sensitive lean mice [44]
IL-1β Produced by macrophages. Implicated in the development of obesity-associated insulin resistance through inhibition of insulin signal transduction [45]
TNF-α Expressed and secreted by adipose tissue. Levels associated with degree of adiposity and insulin resistance. Targeting TNF-α and/or its receptors has been suggested as a promising treatment for insulin resistance and type 2 diabetes mellitus [46]
Nrf2 Involved in resistance to oxidative stress. Functions as a xenobiotic-activated receptor (XAR) to regulate the adaptive response to oxidants [47, 48]
IL-6 Pleiotropic cytokine. A central player in the regulation of inflammation, hematopoiesis, immune responses, and host defense mechanisms. Influences secretion of adipokines from adipocytes. Involved in the etiology of obesity-related comorbidities, including insulin resistance and accelerated atherosclerosis, in humans [51,52,53]
iNOS Synthesizes large quantities of nitric oxide (NO), which acts with reactive oxidative species to producing nitrosative stress, thus playing a key role in adipocyte function and glucose tolerance [54,55,56]
CD 40 Ameliorates inflammation in visceral adipose tissue. Attenuates obesity-induced insulin resistance [49]
CD 80 Plays a homeostatic role in preventing adipose inflammation [50]
ICAM-1 Levels increased in obesity. Positively correlated with central adiposity and insulin resistance [50, 51]
CD 163 Marker of macrophages with anti-inflammatory properties. Increased basal CD163 levels are related to obesity and its metabolic complications [60, 61]
CD 206 Marker of M2-like macrophages in adipose tissues. Inhibits growth and differentiation of adipocyte progenitors, thus controlling adiposity and systemic insulin sensitivity [62]
Arginase Marker of M2 macrophages. Also expressed in endothelial cells. Involved in obesity-induced vascular dysfunction [63, 64]
IL-10 Anti-inflammatory cytokine. High levels found in obese women. Low levels are associated with the metabolic syndrome [65]
IL-1RA Indirectly elicits an anti-inflammatory response. Competitively binds to the IL-1 receptor on the cell surface, thereby inhibiting the inflammatory effects of IL-1 [57,58,59]
TGF-β1 Anti-inflammatory cytokine. Counteracts the effects of the pro-inflammatory cytokines such as IL-8. Inhibits differentiation of pre-adipocytes [66,67,68]
Bax, Bcl-2 Part of the Bcl-2 family of proteins, which constitute a cell-death pathway. Bcl-2 is a death antagonist, and Bax, a death agonist. The setpoint that determines cell susceptibility to apoptosis is determined by the ratio of these molecules. Related to brown adipose tissue atrophy (BAT) in obesity, in part due to apoptosis of adipocytes [69, 70]
Caspase 3 and Caspase 9 Mediate the inflammatory response and apoptotic cell death to maintain homeostasis. Caspase-dependent apoptosis is involved in the pathogenesis of obesity and progression of severe nonalcoholic steatohepatitis (NASH). Caspase 9 is an initiator and caspase 3 is an executioner of cell death [71,72,73]
  1. MMP-2 metalloproteinase-2, ECM extracellular matrix, MMP-9 metalloproteinase-9, CXCR2 CXC chemokine receptor 2, IL-12 interleukin-12, CCL3 C–C motif chemokine ligand 3, MIP-1 macrophage inflammatory protein, CCL2 C–C motif chemokine ligand 2, MCP1 monocyte chemoattractant protein-1, IL-1β interleukin-1β, TNF-α tumor necrosis factor alpha, Nrf2 nuclear factor (erythroid-derived 2)-like 2, IL-6 interleukin-6, iNOS inducible nitric oxide synthase, CD 40 cluster of differentiation 40, CD 80 cluster of differentiation 80, ICAM-1 intercellular adhesion molecule 1, CD 163 cluster of differentiation 163, CD 206 cluster of differentiation 206, IL-10 interleukin-10, IL-1RA interleukin 1 receptor antagonist, TGF-β1 transforming growth factor beta 1, Bax BCL2-associated X, Bcl-2 B-cell lymphoma 2