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Metabolic Recovery with the Persistence of Proinflammatory Leucocyte Dysfunction After Bariatric Intervention for Obesity

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Abstract

Purpose

A suitable option for severe obesity treatment is a surgical approach. After surgery, metabolic markers and weight frequently return to adequate values; however, concerning systemic inflammatory mediators, the results are inconsistent. Furthermore, it has been suggested that leucocyte function may be affected even after weight normalization.

This study aimed to determine if the surgical treatment of obesity influences the production of cytokines by LPS-stimulated as a function of leucocytes.

Materials and Methods

We performed a cross-sectional study that investigated the production of cytokines in response to lipopolysaccharide (LPS) along a kinetic of simulation by leucocytes recovered from individuals with normal weight (NW, n = 8), persons living with obesity (Ob, n = 7), persons living with obesity and diabetes mellitus (Ob-DM, n = 17), and persons that used to live with obesity who underwent bypass surgery (fOb + bypass, n = 8) and recover normal weigh.

Results

IL-6 levels were significantly higher in the Ob and fOb + bypass groups than in NW (p = 0.043). IL-10 secretion without LPS was significantly higher in the NW group than in the other groups explored (p < 0.05). When exposed to LPS, the IL-10 levels increased in all groups except the NW group. As also observed for IL-18 and IL-33, the secretion curve of the fOb + bypass group was more similar to the Ob group, even when they had reached normal weight, as opposed to the NW group.

Conclusion

Our results show that in patients with fOb + bypass, inflammatory and anti-inflammatory cytokine production dynamics remain disrupted even with improved metabolic control and normal weight recovery.

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Data Availability

All data are available from the corresponding author upon request.

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Acknowledgements

All the authors acknowledge and appreciate the hard work of the M.Sc. Esteban Domínguez-Cerezo for helping with data collection. We recognize and thank the bariatric surgeons: Dr. Enrique Luque de León and Dr. Arturo Rodríguez González, from the Gastrointestinal Surgery Department, UMAE Hospital de Especialidades-IMSS, for referencing the included patients. We also thank Dr. Constantino López-Macías for carefully reviewing the different versions of the manuscript. We appreciate the technical support of Jessica L. Prieto-Chávez at the Cytometry Laboratory of the Health Research Coordination (CIS), located at CMN Siglo XXI of the IMSS.

Funding

The study was supported by the FIS/IMSS/PROT/G16/1579 grant from IMSS granted to EFO.

Author information

Authors and Affiliations

  1. Laboratorio de La Dirección de Investigación, Hospital General de México “Dr. Eduardo Liceaga”, Zip Code 06720, Mexico City, Mexico

    Arturo Cérbulo-Vázquez

  2. Applied Immunology Laboratory, National School of Biological Sciences, National Polytechnic Institute, Zip Code 11340, Mexico City, Mexico

    Libier Cabrera-Rivera

  3. Programa de Posgrado en Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Zip Code 11340, Mexico City, Mexico

    Libier Cabrera-Rivera

  4. Departamento de Infectología E Inmunología, Instituto Nacional de Perinatología, Zip Code 11000, Mexico City, Mexico

    Ismael Mancilla-Herrera

  5. Department of Clinical Research, Investigador por México, Consejo Nacional de Humanidades Ciencias y Tecnologías (CONAHCyT), Instituto Nacional de Cancerología, Zip Code 14080, Mexico City, Mexico

    Denisse Castro-Eguiluz

  6. Laboratorio de Inmunorregulación, Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Zip Code 11340, Mexico City, Mexico

    Francisco J. Sánchez-García

  7. División de Investigación Clínica de La Coordinación de Investigación en Salud, Instituto Mexicano del Seguro Social, Zip Code 06720, Mexico City, Mexico

    Eduardo A. Ferat-Osorio

  8. Unidad de Investigación Médica en Inmunoquímica, UMAE Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Av. Cuauhtémoc 330, 06720, Zip Code 06720, Mexico City, Mexico

    Lourdes A. Arriaga-Pizano

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  1. Arturo Cérbulo-Vázquez
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Contributions

LAAP, EFO, and FJSG proposed and discussed the seed idea. EFO and LCR recollected the samples and filled the database. LCR treated the samples and performed stimulation assays. ACV, LCR, IMH, and LAAP performed flow cytometry analysis for leucocyte immunophenotyping and cytokine/chemokine immunoassays. ACV, IMH, and LAAP performed statistical analysis. ACV and DCE organized data and wrote the first draft of the manuscript. All authors have read and approved the final version of the manuscript.

Corresponding author

Correspondence to Lourdes A. Arriaga-Pizano.

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Key Points

• Disrupted leucocyte response to LPS remains after bariatric surgery.

• Bariatric surgery induces metabolic control but does not recover leucocyte function.

• Deregulated cytokine production even after weight normalization/bypass surgery.

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Cérbulo-Vázquez, A., Cabrera-Rivera, L., Mancilla-Herrera, I. et al. Metabolic Recovery with the Persistence of Proinflammatory Leucocyte Dysfunction After Bariatric Intervention for Obesity. OBES SURG 34, 1575–1583 (2024). https://doi.org/10.1007/s11695-024-07135-2

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