Evidence for anti-inflammatory effects of exercise in CKD.
CKD is associated with a complex state of immune dysfunction characterized by immune depression, predisposing patients to infections, and immune activation, resulting in inflammation that associates with higher risk of cardiovascular disease. Physical exercise may enhance immune function and exert anti-inflammatory effects, but such effects are unclear in CKD. We investigated the separate effects of acute and regular moderate-intensity aerobic exercise on neutrophil degranulation (elastase release), activation of T lymphocytes (CD69 expression) and monocytes (CD86 and HLA-DR expression), and plasma inflammatory markers (IL-6, IL-10, soluble TNF-receptors, and C-reactive protein) in patients with predialysis CKD. A single 30-minute (acute) bout of walking induced a normal pattern of leukocyte mobilization and had no effect on T-lymphocyte and monocyte activation but improved neutrophil responsiveness to a bacterial challenge in the postexercise period. Furthermore, acute exercise induced a systemic anti-inflammatory environment, evidenced by a marked increase in plasma IL-10 levels (peaked at 1 hour postexercise), that was most likely mediated by increased plasma IL-6 levels (peaked immediately postexercise). Six months of regular walking exercise (30 min/d for 5 times/wk) exerted anti-inflammatory effects (reduction in the ratio of plasma IL-6 to IL-10 levels) and a downregulation of T-lymphocyte and monocyte activation, but it had no effect on circulating immune cell numbers or neutrophil degranulation responses. Renal function, proteinuria, and BP were also unaffected. These findings provide compelling evidence that walking exercise is safe with regard to immune and inflammatory responses and has the potential to be an effective anti-inflammatory therapy in predialysis CKD.
School of Sport, Exercise and Health Sciences, Loughborough University, Leicestershire, United Kingdom; j.viana@lboro.ac.uk.
João L
JL
Viana
John Walls Renal Unit, Leicester General Hospital, Leicester, United Kingdom; and.
George C
GC
Kosmadakis
Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
Emma L
EL
Watson
Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
Alan
A
Bevington
John Walls Renal Unit, Leicester General Hospital, Leicester, United Kingdom; and.
John
J
Feehally
School of Sport, Exercise and Health Sciences, Loughborough University, Leicestershire, United Kingdom;
Nicolette C
NC
Bishop
John Walls Renal Unit, Leicester General Hospital, Leicester, United Kingdom; and Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
Alice C
AC
Smith
D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D015444:Exercise / Q000502:physiology*; D005081:Exercise Therapy; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D018375:Neutrophil Activation; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood; D051436:Renal Insufficiency, Chronic / Q000276:immunology* / Q000628:therapy; D013601:T-Lymphocytes / Q000276:immunology; D016138:Walking / Q000502:physiology
C508609:IL10 protein, human; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D016753:Interleukin-10; D002097:C-Reactive Protein