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Neutrophil extracellular traps (NETs) modulate inflammatory profile in obese humans and mice: adipose tissue role on NETs levels.

Authors :
Freitas DF
Colón DF
Silva RL
Santos EM
Guimarães VHD
Ribeiro GHM
de Paula AMB
Guimarães ALS
Dos Reis ST
Cunha FQ
Antunes MM
Menezes GB
Santos SHS
Source :
Molecular biology reports [Mol Biol Rep] 2022 Apr; Vol. 49 (4), pp. 3225-3236. Date of Electronic Publication: 2022 Jan 22.
Publication Year :
2022

Abstract

Background: Neutrophil extracellular traps (NETs) are a recently discovered neutrophil defense mechanism which modulates several inflammatory conditions contributing to metabolic profile alterations. Therefore, the present study aimed to evaluate the production of NETs in obese patients and mice, verifying the possible mechanisms associated with the release of NETs by the adipose tissue.<br />Methods and Results: The present study investigated NETs production in human adipose tissue and also showing the neutrophils using intravital microscopy in mouse epididymal adipose tissue. Blood and white adipose tissues were obtained from eutrophic and obese individuals and from mice. Lipid, glycemic and leukocyte profiles were evaluated, as well as the levels of NETs and its markers. Bioinformatics and proteomics analyses were performed and the identified key proteins were measured. The main findings showed that the inflammatory markers interleukin-8 (IL-8), heat shock protein 90 (HSP90) and the E1 heat shock protein family (HSPE1) can be modulated by the NETs levels in obesity. Obesity has also been associated with increased cholesterol, glucose intolerance, ionic calcium and NETs. We also observed an increase in catalase and a decreased superoxide dismutase activity. Bioinformatics and proteomics analyses revealed that IL-8, HSP90 and HSPE1 were associated with obesity, inflammation and NETs release.<br />Conclusions: In conclusion, the present study shows an increase in NETs production during obesity associated with important inflammatory markers in adipose.<br /> (© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

Details

Language :
English
ISSN :
1573-4978
Volume :
49
Issue :
4
Database :
MEDLINE
Journal :
Molecular biology reports
Publication Type :
Academic Journal
Accession number :
35066770
Full Text :
https://doi.org/10.1007/s11033-022-07157-y