Ricardo X Cuellar-Tamez1, J Romeo Villarreal-Calderon1, Nestor Rubio-Infante1, Elena C Castillo1, Manuel García-Garza2, Leticia Elizondo-Montemayor3,4, Gerardo García-Rivas5,6,7. 1. Tecnologico de Monterrey, Escuela de Medicina Y Ciencias de La Salud, Ave. Morones Prieto 3000, Monterrey, NL, 64710, Mexico. 2. Swiss Hospital, SMG, Monterrey, NL, Mexico. 3. Tecnologico de Monterrey, Escuela de Medicina Y Ciencias de La Salud, Ave. Morones Prieto 3000, Monterrey, NL, 64710, Mexico. lelizond@tec.mx. 4. Tecnologico de Monterrey, Centro de Investigación en Nutrición Clínica Y Obesidad, Monterrey, NL, Mexico. lelizond@tec.mx. 5. Tecnologico de Monterrey, Escuela de Medicina Y Ciencias de La Salud, Ave. Morones Prieto 3000, Monterrey, NL, 64710, Mexico. gdejesus@tec.mx. 6. Tecnologico de Monterrey, Centro de Investigación Biomédica, Hospital Zambrano Hellion, TecSalud, 66278, San Pedro Garza García, NL, Mexico. gdejesus@tec.mx. 7. Tecnologico de Monterrey, Centro de Medicina Funcional, Hospital Zambrano Hellion, TecSalud, 66278, San Pedro Garza García, NL, Mexico. gdejesus@tec.mx.
Abstract
BACKGROUND: Obesity is associated with a chronic inflammatory state and autoimmune diseases, but little is known about the role of B cells in this context and the changes in B cell activation factors during obesity and after weight loss. To test whether bariatric-surgery-induced weight loss ameliorates the systemic inflammatory state associated with B cell activation molecules. METHODS: We conducted a prospective observational study in patients treated with bariatric surgery. Anthropometric and body composition measurements were performed preoperatively and at 6 months of follow-up post surgery. The patients were tested for a biochemical profile, plasmatic immunoglobulin G (IgG), cytokines (including specific B cell activating cytokines), and adipokines serum levels RESULTS: The patients' weight loss was accounted for mostly by fat mass (52.9%). We observed a significant reduction in total plasmatic IgG levels (p = 0.001), which could be associated with decreased B cell activity. Accordingly, there was a significant decrease in the B cell activating factors such as APRIL, BAFF, and soluble CD40L and a general improvement in the inflammatory markers hs-CRP, IL-1β, IL-12, IL-18, and IFN-γ. CONCLUSIONS: These findings point toward reduced B cell activity after weight loss due to bariatric surgery. Moreover, they could be the initial link among the systemic inflammatory factors, and B cell activation in this inflammatory context that leads to IgG production and, potentially, to autoimmunity in patients with severe obesity.
BACKGROUND:Obesity is associated with a chronic inflammatory state and autoimmune diseases, but little is known about the role of B cells in this context and the changes in B cell activation factors during obesity and after weight loss. To test whether bariatric-surgery-induced weight loss ameliorates the systemic inflammatory state associated with B cell activation molecules. METHODS: We conducted a prospective observational study in patients treated with bariatric surgery. Anthropometric and body composition measurements were performed preoperatively and at 6 months of follow-up post surgery. The patients were tested for a biochemical profile, plasmatic immunoglobulin G (IgG), cytokines (including specific B cell activating cytokines), and adipokines serum levels RESULTS: The patients' weight loss was accounted for mostly by fat mass (52.9%). We observed a significant reduction in total plasmatic IgG levels (p = 0.001), which could be associated with decreased B cell activity. Accordingly, there was a significant decrease in the B cell activating factors such as APRIL, BAFF, and soluble CD40L and a general improvement in the inflammatory markers hs-CRP, IL-1β, IL-12, IL-18, and IFN-γ. CONCLUSIONS: These findings point toward reduced B cell activity after weight loss due to bariatric surgery. Moreover, they could be the initial link among the systemic inflammatory factors, and B cell activation in this inflammatory context that leads to IgG production and, potentially, to autoimmunity in patients with severe obesity.
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