Reduced Th1 response is associated with lower glycolytic activity in activated peripheral blood mononuclear cells after metabolic and bariatric surgery

Background Obesity promotes cellular immunometabolism changes that trigger the activation of macrophages and lymphocytes, leading to systemic inflammation. Activated leukocytes undergo metabolic reprogramming, increasing glycolytic activity. Objective To examine whether the reduction in the inflamma...

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Veröffentlicht in:Journal of endocrinological investigation 2021-12, Vol.44 (12), p.2819-2830
Hauptverfasser: Villarreal-Calderón, J. R., Castillo, E. C., Cuellar-Tamez, R. X., García-Garza, M., Elizondo-Montemayor, L., García-Rivas, G.
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Sprache:eng
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Zusammenfassung:Background Obesity promotes cellular immunometabolism changes that trigger the activation of macrophages and lymphocytes, leading to systemic inflammation. Activated leukocytes undergo metabolic reprogramming, increasing glycolytic activity. Objective To examine whether the reduction in the inflammatory state associated with bariatric surgery is associated with decreased glycolytic activity in leukocytes. Setting Single-center, prospective observational study. Methods This study involved 18 patients with obesity undergoing bariatric surgery. All measurements were performed preoperatively and six months postoperatively. Peripheral blood mononuclear cells and plasma were obtained to determine the glycolytic rate and mitochondrial membrane potential as surrogates of the metabolic switching and high-sensitivity C-reactive protein, adipokines, and CD69 expression as inflammatory and activation markers. Results Glycolytic activity engaged by CD3/CD28 activation was reduced six months after bariatric surgery, associated with decreased levels of T helper (Th) 1 and Th17 signature cytokines. An overall reduction in inflammatory markers was observed, which correlated with a higher adiponectin/leptin ratio. Conclusions Metabolic and bariatric surgery-induced weight loss leads to reprogramming in T cells’ metabolic machinery, resulting in reduced stimulation of glycolysis after activation, which may explain the decrease in systemic inflammation mediated by cytokines such as interferon-γ and interleukin-17A.
ISSN:1720-8386
0391-4097
1720-8386
DOI:10.1007/s40618-021-01587-4