The Role of NLRP1, AIM2 and MEFV Inflammasomes in the High-Intensity Interval Training of Individuals With Obesity.

IF 5 3区 医学 Q2 IMMUNOLOGY
Immunology Pub Date : 2026-05-01 Epub Date: 2025-12-21 DOI:10.1111/imm.70090
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, Marina Tiemi Shio, Paula Rezende-Teixeira, Carolina Nunes França
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引用次数: 0

Abstract

Obesity is a chronic disease associated with systemic inflammation caused by excess visceral fat and pro-inflammatory cytokines such as IL-1β and IL-6. Inflammasomes-particularly those involving genes such as NLRP1, AIM2 and MEFV-play a key role in this process. High-intensity interval training (HIIT) can counteract this inflammation; however, it remains unclear how HIIT modulates inflammasome gene expression in obesity. This study investigated whether HIIT can alter the expression of genes related to the inflammasomes NLRP1, AIM2 and MEFV in obese individuals. The results showed that, after 8 weeks of HIIT, there was an increase in the expression of the genes AIM2, MEFV, CARD16 and CARD18. The increase in CARD16, known to inhibit caspase-1 dimerisation, reinforces the hypothesis related to decreased inflammation, evidenced by the absence of clear activation of the NLRP1 inflammasome and by lower serum IL-1β concentrations in trained participants. Although CARD18 was also upregulated, its function remains ambiguous, and it may act as an inhibitor or modulator of inflammation. Therefore, we conclude that HIIT is a promising intervention for modulating inflammatory genes in individuals with obesity, with the potential to reduce systemic inflammation and its pathological effects.

NLRP1, AIM2和MEFV炎症小体在肥胖个体高强度间歇训练中的作用
肥胖是一种慢性疾病,与内脏脂肪过多和促炎细胞因子如IL-1β和IL-6引起的全身性炎症有关。炎症小体——尤其是涉及NLRP1、AIM2和mefv等基因的炎症小体——在这一过程中起着关键作用。高强度间歇训练(HIIT)可以对抗这种炎症;然而,HIIT如何调节肥胖中的炎性体基因表达仍不清楚。本研究探讨了HIIT是否可以改变肥胖个体炎症小体NLRP1、AIM2和MEFV相关基因的表达。结果显示,HIIT 8周后,AIM2、MEFV、CARD16、CARD18基因表达增加。已知能抑制caspase-1二聚化的CARD16的增加,强化了与炎症减少有关的假设,这可以通过NLRP1炎症小体缺乏明显激活和训练参与者血清IL-1β浓度降低来证明。虽然CARD18也上调,但其功能尚不明确,可能作为炎症的抑制剂或调节剂。因此,我们得出结论,HIIT是一种很有希望的干预措施,可以调节肥胖个体的炎症基因,有可能减少全身炎症及其病理影响。
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来源期刊
Immunology
Immunology 医学-免疫学
CiteScore
11.90
自引率
1.60%
发文量
175
审稿时长
4-8 weeks
期刊介绍: Immunology is one of the longest-established immunology journals and is recognised as one of the leading journals in its field. We have global representation in authors, editors and reviewers. Immunology publishes papers describing original findings in all areas of cellular and molecular immunology. High-quality original articles describing mechanistic insights into fundamental aspects of the immune system are welcome. Topics of interest to the journal include: immune cell development, cancer immunology, systems immunology/omics and informatics, inflammation, immunometabolism, immunology of infection, microbiota and immunity, mucosal immunology, and neuroimmunology. The journal also publishes commissioned review articles on subjects of topical interest to immunologists, and commissions in-depth review series: themed sets of review articles which take a 360° view of select topics at the heart of immunological research.
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