Exercise intensity and training alter the innate immune cell type and chromosomal origins of circulating cell- free DNA in humans

• 成果类型: Article
• 署名作者: Rodrigues, Kameron B.; Weng, Ziming; Graham, Zachary A.; Lavin, Kaleen; Mcadam, Jeremy; Tuggle, S. Craig; Peoples, Brandon; Seay, Regina; Yang, Sufen; Bamman, Marcas M.; Broderick, Timothy J.; Montgomery, Stephen B.
• 署名单位: Stanford University; Florida Institute for Human & Machine Cognition (IHMC); University of Alabama System; University of Alabama Birmingham
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-14337
• DOI: 10.1073/pnas.2406954122
• 发表日期: 2025-01-21
• 关键词: neutrophil extracellular traps; free plasma dna; mitochondrial-dna; physical-activity; release; methylation; increases; kinetics; expression; infection

摘要

Exercising regularly promotes health, but these benefits are complicated by acute inflammation induced by exercise. A potential source of inflammation is cell- free DNA (cfDNA), yet the cellular origins, molecular causes, and immune system interactions of exercise- induced cfDNA are unclear. To study these, 10 healthy individuals were randomized to a 12- wk exercise program of either high- intensity tactical training (HITT) or traditional moderate- intensity training (TRAD). Blood plasma was collected pre- and postexercise at weeks 0 and 12 and after 4 wk of detraining upon program completion. deconvolution was applied to cfDNA obtained from the 50 plasma samples and paired release of cfDNA from neutrophils, dendritic cells (DCs), and macrophages proportional to exercise intensity. Exercise training reduced cfDNA released in HITT participants but training lowered mitochondrial cfDNA at rest, even after detraining. Using a sequencing where cells release DNA extracellular traps, was the likely source of cfDNA, demonstrated by enrichment of nuclear DNA. Further, several cytokines were induced by acute to the anti- inflammatory effects of regular exercise.