# The effects of high-intensity interval training on NLRP3 inflammasome and monocyte chemokine receptors in individuals with obesity

**Authors:** Ana Luíza Pereira Assunção Silveira, Daniela Alves de Abreu, Amanda de Lima Santos Musto, Luiz Henrique da Silva Nali, Jônatas Bussador do Amaral, André Luis Lacerda Bachi, Lucas Melo Neves, Saulo Gil, Fernando Mateus Santos, Jefferson Russo Victor, Marina Tiemi Shio, Carolina Nunes França

PMC · DOI: 10.1371/journal.pone.0343214 · PLOS One · 2026-02-23

## TL;DR

This study shows that high-intensity interval training can reduce inflammation in people with obesity by affecting specific immune-related genes and receptors.

## Contribution

The study reveals how HIIT modulates the NLRP3 inflammasome and monocyte chemokine receptors in individuals with obesity.

## Key findings

- HIIT decreased Caspase-1 and IL-6 expression while increasing ASC expression in individuals with obesity.
- HIIT increased CCR2 and CCR5 expression and decreased CX3CR1 expression in monocyte chemokine receptors.
- Differentially expressed genes showed interaction with NLRP3 inflammasome genes after HIIT.

## Abstract

Background/ Objectives: Obesity is a chronic disease that promotes increased cytokine production mediated by activating a complex of intracellular proteins known as the inflammasome, mainly NLRP3. The modulation of the NLRP3 inflammasome and monocyte chemokine receptors induced by high-intensity interval training (HIIT) in individuals with obesity is still poorly understood. This training is characterized by a period of high-intensity stimulation followed by a recovery period. The main objective of the current study was to investigate possible modulation of the NLRP3 inflammasome and monocyte chemokine receptors in individuals with obesity following HIIT. Subjects/Methods: In this randomized trial, we included individuals with obesity (n = 109), who have not exercised in the last six months, of both sexes, aged between 18 and 60 years. Interventions: Participants were divided into a trained group, which performed three weekly HIIT sessions over eight weeks, and an untrained group (control). The NLRP3 inflammasome and its components, as well as monocyte chemokine receptors expression were analyzed before and after training period by real-time PCR. Results: Whereas NLRP3 expression were unchanged (p = 0.08), after HIIT there was a decrease in Caspase-1 (CASP-1) expression in contrast to the increase of ASC expression as compared to baseline values (p = 0.04 and p < 0.0001, respectively). Additionally, lower IL-6 expression (p < 0.0001), with no differences in IL-1 β and IL-18 expressions were found after HIIT. Besides, HIIT led to an increase in the expression of CCR2 and CCR5 and a decrease in CX3CR1 expression (p < 0.0001, p = 0.001 and p = 0.007, respectively) compared to baseline. Differentially expressed genes interaction analysis [CASP-1, ASC (PYCARD), IL-6, CCR2, CXC3CR1 and CCR5] revealed interaction with NLRP3 nflammasome genes. Conclusions: Eight weeks of HIIT can modulate some components involved in the NLRP3 inflammasome, as well as monocyte chemokine receptors, in individuals with obesity, suggesting an improvement in the control of inflammatory status. Trial registration: Brazilian Registry of Clinical Trials – ReBEC number RBR-8vfxfqd).

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548], CASP1 (caspase 1) [NCBI Gene 834], STS (steroid sulfatase) [NCBI Gene 412], IL6 (interleukin 6) [NCBI Gene 3569], CCR2 (C-C motif chemokine receptor 2) [NCBI Gene 729230], CCR5 (C-C motif chemokine receptor 5) [NCBI Gene 1234], IL1B (interleukin 1 beta) [NCBI Gene 3553], IL18 (interleukin 18) [NCBI Gene 3606]
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, CHUK (component of inhibitor of nuclear factor kappa B kinase complex) [NCBI Gene 1147] {aka BPS2, IKBKA, IKK-1, IKK-alpha, IKK1, IKKA}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, IL18 (interleukin 18) [NCBI Gene 3606] {aka IGIF, IL-18, IL-1g, IL1F4}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, CASP1 (caspase 1) [NCBI Gene 834] {aka ICE, IL1BC, P45}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, NLRP1 (NLR family pyrin domain containing 1) [NCBI Gene 22861] {aka AIADK, CARD7, CIDED, CLR17.1, DEFCAP, DEFCAP-L/S}, PYCARD (PYD and CARD domain containing) [NCBI Gene 29108] {aka ASC, CARD5, TMS, TMS-1, TMS1}, ISYNA1 (inositol-3-phosphate synthase 1) [NCBI Gene 51477] {aka INO1, INOS, IPS, IPS 1, IPS-1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CCR5 (C-C motif chemokine receptor 5) [NCBI Gene 1234] {aka CC-CKR-5, CCCKR5, CCR-5, CD195, CKR-5, CKR5}, CCR2 (C-C motif chemokine receptor 2) [NCBI Gene 729230] {aka CC-CKR-2, CCR-2, CCR2A, CCR2B, CD192, CKR2}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, CX3CR1 (C-X3-C motif chemokine receptor 1) [NCBI Gene 1524] {aka CCRL1, CMKBRL1, CMKDR1, GPR13, GPRV28, V28}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, IKBKB (inhibitor of nuclear factor kappa B kinase subunit beta) [NCBI Gene 3551] {aka IKK-2, IKK-beta, IKK2, IKKB, IMD15, IMD15A}, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}, SYK (spleen associated tyrosine kinase) [NCBI Gene 6850] {aka IMD82, p72-Syk}, NLRC4 (NLR family CARD domain containing 4) [NCBI Gene 58484] {aka AIFEC, CARD12, CLAN, CLAN1, CLANA, CLANB}
- **Diseases:** inflammation (MESH:D007249), metabolic (MESH:D008659), HIIT (MESH:D000095027), Obesity (MESH:D009765), overweight (MESH:D050177), cardiovascular disease (MESH:D002318), insulin resistance (MESH:D007333), atherogenesis (MESH:D050197), immunodeficiency (MESH:D007153), protein malnutrition (MESH:D044342), PE (MESH:D000092202), chronic (MESH:D002908), heart failure (MESH:D006333), adipose tissue (MESH:D018205), type 2 diabetes (MESH:D003924), inflammatory cytokines (MESH:D000080424)
- **Chemicals:** ammonium chloride (MESH:D000643), uric acid (MESH:D014527), EDTA (MESH:D004492), triglyceride (MESH:D014280), glycemia (MESH:D001786), ceramide (MESH:D002518), cholesterol (MESH:D002784), Trizol (MESH:C411644), peroxide (MESH:D010545), PA (MESH:D010168), DEXA (-), ROS (MESH:D017382), glucose (MESH:D005947), Lipid (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

45 references — full list in the complete paper: https://tomesphere.com/paper/PMC12928487/full.md

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Source: https://tomesphere.com/paper/PMC12928487