The Chemokine Systems at the Crossroads of Inflammation and Energy Metabolism in the Development of Obesity

Abstract

Obesity is characterized as a complex and multifactorial excess accretion of adipose tissue accompanied with alterations in the immune and metabolic responses. Although the chemokine systems have been documented to be involved in the control of tissue inflammation and metabolism, the dual role of chemokines and chemokine receptors in the pathogenesis of the inflammatory milieu and dysregulated energy metabolism in obesity remains elusive. The objective of this review is to present an update on the link between chemokines and obesity-related inflammation and metabolism dysregulation under the light of recent knowledge, which may present important therapeutic targets that could control obesity-associated immune and metabolic disorders and chronic complications in the near future. In addition, the cellular and molecular mechanisms of chemokines and chemokine receptors including the potential effect of post-translational modification of chemokines in the regulation of inflammation and energy metabolism will be discussed in this review.

Prolonged Antiretroviral Treatment Induces Adipose Tissue Remodelling Associated with Mild Inflammation in SIV-Infected Macaques

“…Lastly, we studied the mRNA expression of genes coding for chemokines that contribute to the inflammatory processes by recruiting immune cells and prompting the latter to generate pro-inflammatory signals. With regard to the mRNA expression of standard markers of macrophage recruitment (MCP1, CCL5, and CXCL10), T cell recruitment (CX3CL1 and CXCL10) and NK cell recruitment (CX3CL1), we did not observe any significant changes in SIV+ animals versus SIV− animals [39,40]. Although the significant difference in MCP1 expression have been widely reported in the context of obesity [41], we In summary, we detected few differences in the AT's production of these two cytokines following infection.…”

Identification of the critical genes and signaling pathways in subcutaneous adipose tissue after bariatric surgery based on the GEO database

“…GSEA reveals that, before bariatric surgery, most genes are predominantly enriched in chemokines, TOLL-like receptor, and B cell receptor signaling pathways-mechanisms integral to adipose tissue in ammation. Adipocytes release chemokines that intensify tissue in ammation, with speci c chemokines like CCL2 and CCL5 exacerbating systemic in ammation by recruiting proin ammatory M1 macrophages, thereby contributing to obesity and its chronic complications [21]. Toll-like receptor signaling induces fatty acid synthesis, fostering chronic in ammation in adipose tissue and contributing to the metabolic syndrome associated with obesity [22].…”

3-OH Phloretin Inhibits High-Fat Diet-Induced Obesity and Obesity-Induced Inflammation by Reducing Macrophage Infiltration into White Adipose Tissue

“…Indeed, several studies have reported that the deficiency of M1 macrophages enhances insulin sensitivity in obese mice [ 38 ], whereas deletion of M2 macrophages results in insulin resistance in wild-type (WT) mice [ 38 ]. Obesity induces upregulated expression of chemokines such as MCP-1 (monocyte chemoattractant protein-1, CCL2) and CCL5 (C-C Motif Chemokine Ligand 5) in order to recruit M1 macrophages to adipose tissues [ 39 ]. These recruited M1 macrophages secrete pro-inflammatory cytokines, including TNF, IL-6, and IL-1β, and oxidative metabolites such as superoxide and nitric oxide (NO), resulting in inflammation and insulin resistance [ 40 , 41 ].…”