Exercise elevates plasma levels but not gene expression of IL-1β, IL-6, and TNF-α in blood mononuclear cells

Moldoveanu, Andrei; Shephard, Roy J.; Shek, Pang N.

doi:10.1152/jappl.2000.89.4.1499

Cited by 197 publications

(172 citation statements)

References 30 publications

Supporting

Mentioning

140

Contrasting

Unclassified

Order By: Relevance

“…Being certain that monocytes are the main source of Il-6 during common immune response during sepsis or local infections, the first hypothesis tested was that immune cells were responsible of IL-6 increase during exercise [166], but early different groups demonstrated that IL-6 mRNA in monocytes did not increase as a result of exercise [167,168]. These and other subsequent works clearly demonstrated that monocytes are not the source of the exercise-induced increase in plasma IL-6.…”

Section: Acute Changes Of Systemic Inflammatory Markers During and Afmentioning

confidence: 99%

Effects of Physical Exercise on Inflammatory Markers of Atherosclerosis

Pinto¹,

Raimondo

Tuttolomondo³

et al. 2012

CPD

View full text Add to dashboard Cite

Abstract:It is well established that physically fit individuals have a reduced risk of developing CVD (cardiovascular disease) and other age-related chronic disorders. Regular exercise is an established therapeutic intervention with an enormous range of benefits. Chronic low-grade systemic inflammation may be involved in atherosclerosis, diabetes and in pathogenesis of several chronic pathological conditions; recent findings confirm that physical activity induces an increase in the systemic levels of a number of cytokines and chemokines with anti-inflammatory properties. The possibility that regular physical exercise exerts anti-inflammation activity, being the interaction between contracting muscle and the other tissues and the circulating cells mediated through signals transmitted by "myokines" produced with muscle contractions. To date the list of myokines includes IL-6, IL-8, and IL-15. During muscle contractions are also released IL1receptor antagonis and sTNF-R, molecules that contribute to provide anti-inflammatory actions.Nevertheless discrepancies, analysis of available researches seem to confirm the efficacy of regular physical training as a nonpharmacological therapy having target chronic low-grade inflammation. Given this, physical exercise could be considerate a useful weapon against local vascular and systemic inflammation in atherosclerosis. Several mechanisms explain the positive effect of chronic exercise, nevertheless, these mechanisms do not fully enlighten all pathways by which exercise can decrease inflammation and endothelial dysfunction, and hence modulate the progression of the underlying disease progress.

show abstract

Section: Acute Changes Of Systemic Inflammatory Markers During and Afmentioning

confidence: 99%

Effects of Physical Exercise on Inflammatory Markers of Atherosclerosis

Pinto¹,

Raimondo

Tuttolomondo³

et al. 2012

CPD

View full text Add to dashboard Cite

show abstract

“…However, many investigations have shown that the practice of moderate exercises induces a Th1 response, with production of pro-inflammatory cytokines 48,59,81 . Resistance exercises of moderate intensity induced a light systemic inflammatory response, which is characterized, at least partly, by increases in the serum levels of inflammatory cytokines, such as IL1β and TNF-α 95,96 . Keller et al 97 reported that the TNF-α super-expression returned to normal concentrations after 1h of acute swimming exercise in mice whose TNF-α (TNFR) gene receptor was deleted.…”

Section: Effect Of Physical Exercise In the Cytokine Productionmentioning

confidence: 99%

Efeito do exercício no sistema imune: resposta, adaptação e sinalização celular

Terra

Da-Silva

Salerno

et al. 2012

Rev Bras Med Esporte

View full text Add to dashboard Cite

Introduction: Over the last century, people have become less active, adopting more sedentary habits. This scenario has increased the incidence of chronic diseases such as cardiovascular diseases, type 2 diabetes and metabolic syndrome. The practice of physical activities can influence healthiness by altering the metabolic state and also the immune system. Objective: To review the literature for studies that address the effects promoted by physical exercise on the development of immune responses and the possible signal transduction pathways. Methods: The SciELO and PubMed data bases were consulted. Results: The available literature shows that during the practice of exercise, various subpopulations of leukocytes are altered in accordance with the intensity and duration of the activity performed. Exercise of moderate intensity stimulates a pro-inflammatory response, while those of high intensity tend to promote antiinflammatory responses that could decrease damage to skeletal muscle. Such alterations are observed in cells that present antigens (such as macrophages and dendritic cells), neutrophils, natural killer cells (NK) and in surface molecules like Toll-like receptors (TLR) and major histocompatibility complex class II, as well as the entire repertoire of cytokines. Conclusion: The current state of knowledge suggests that the alterations in the immune system are dependent on parameters inherent to exercise and that in order to have all these alterations occurring, some cell signaling cascades are activated, giving rise to a complex process of phosphorylation/dephosphorylation that culminates in the activation of transcription factors, translation of mRNA's, protein synthesis and cell proliferation.

show abstract

“…Given the pattern of expression of eNOS, which is regulated not only at the transcriptional level but also posttranscriptionally (25), it is possible that complex interactions between different endogenous mediators released acutely during exercise constitute the stimulus for several chronic adaptations. High-intensity exercise, as used in the above-mentioned study of Miyauchi et al (34), elicits the release of proinflammatory cytokines such as tumor necrosis factor-␣ (TNF-␣), interleukin (IL)-1␤, and IL-6 (35,40,56). Interestingly, it has been shown that TNF-␣ induces a downregulation of eNOS, which results from a destabilization of eNOS mRNA with no effect on transcription (25,60).…”

Section: Exercise Training and Renal Vascular Reactivitymentioning

confidence: 99%

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

Moraes¹,

Gioseffi²,

Nóbrega³

et al. 2004

Journal of Applied Physiology

View full text Add to dashboard Cite

is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro-and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n ϭ 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n ϭ 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 Ϯ 8% (n ϭ 6; P Ͻ 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 Ϯ 6% (n ϭ 6; P Ͻ 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 Ϯ 8 and 13 Ϯ 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͼ 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with N -nitro-L-arginine methyl ester (L-NAME; 300 M), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 Ϯ 6 and 38 Ϯ 5% for ExT and L-NAME ϩ ExT, respectively (n ϭ 6; P Ͻ 0.05)]. On the other hand, L-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 Ϯ 7 and 45 Ϯ 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͻ 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO. chronic exercise; endothelial dysfunction; isolated perfused rabbit kidney IT IS WELL KNOWN THAT THE endothelium plays a role of paramount importance in the regulation of the vasomotor tone (for review, see Ref. 26). The endothelial cells synthesize and release several relaxing and contracting diffusible substances that interact with the underlying vascular smooth muscle, thus contributing to the continuous modulation of vascular reactivity (26). The best-characterized endothelium-derived relaxing factors are nitric oxide (NO) and prostacyclin (PGI 2 ), which can be released by physical (shear stress by the fl...

show abstract

Exercise elevates plasma levels but not gene expression of IL-1β, IL-6, and TNF-α in blood mononuclear cells

Cited by 197 publications

References 30 publications

Effects of Physical Exercise on Inflammatory Markers of Atherosclerosis

Effects of Physical Exercise on Inflammatory Markers of Atherosclerosis

Efeito do exercício no sistema imune: resposta, adaptação e sinalização celular

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

Contact Info

Product

Resources

About