Pro‐ and anti‐inflammatory cytokine balance in strenuous exercise in humans

Ostrowski, Kenneth; Rohde, Thomas D.; Asp, Sven; Schjerling, Peter; Pedersen, Bente Klarlund

doi:10.1111/j.1469-7793.1999.287ad.x

Cited by 840 publications

(822 citation statements)

References 22 publications

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“…The suppression of the production of these particular pro-inflammatory cytokines is consistent with previous observations by other investigators using different methods to assess the immediate immune consequences of physical activity. Moreover, the data are consistent with the notion that any pro-inflammatory stimulation by exercise is balanced in healthy people by activation of mediators and factors that ultimately attenuate the inflammatory cascade [48]. We were able to identify these responses using only a 10% concentration of human serum and by incubating cells that were "naïve" to the exercise.…”

Section: Discussionsupporting

confidence: 81%

Serum from exercising humans suppresses t-cell cytokine production

Radom‐Aizik¹,

Leu²,

Zaldivar³

2007

Cytokine

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Exercise affects t-cell cytokine production. Whether or not these effects are caused by circulating factors associated with physical activity (e.g., inflammatory mediators, acidosis) is unknown. To investigate this, we incubated sera (10%), obtained from 16 young-adults before (PRE) and after (END) 30-min of exercise, with commercially available Jurkat cells, a t-lymphocyte model, that, of course, had never been exposed to an exercise milieu. After 1-h and 6-h in culture, we measured in the supernatant four cytokines (each known to be altered by exercise and involved in disease pathophysiology): IL-2, TGF-β1, TNF-α, and IL-1ra. Cell proliferation was assessed with proliferating nuclear cell antigen (PNCA). Statistical analysis consisted of a linear mixed model for repeated measurement. There was no effect of exercise on t-cell production of either TGF-β1 or IL-1ra. In contrast, both IL-2 (p=0.025) and TNF-α (p=0.031) production was significantly suppressed in sera from the exercising participants. The suppression of these two cytokines occurred despite the fact that PNCA significantly increased (p<0.0001) in the END serum. In conclusion, exercise alters circulating factors that can, subsequently, influence t-cell cytokine production in vitro.

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Section: Discussionsupporting

confidence: 81%

Serum from exercising humans suppresses t-cell cytokine production

Radom‐Aizik¹,

Leu²,

Zaldivar³

2007

Cytokine

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“…These cytokine are a family of low-molecular weight, cell-to-cell mediators that regulate many immune and inflammatory responses 22) . Previous studies of very strenuous exercise in adult subjects have demonstrated robust increases in the circulating levels of IL-1β, TNF-α and IL-6 [22][23][24] . However, reports showing the levels of this inflammatory cytokines in saliva before, during and after acute exercise are lacking.…”

Section: ⅰ．Introductionmentioning

confidence: 90%

Effects of Acute Prolonged Strenuous Exercise on the Salivary Stress Markers and Inflammatory Cytokines

Usui

Yoshikawa

Ueda

et al. 2011

Jpn. J. Phys. Fitness Sports Med.

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The aim of the present study was to examine whether amount of oral cortisol, immunoglobulin A (IgA), chromogranin A (CgA) and inflammatory cytokines, might be affected by prolonged strenuous exercise. Ten young male volunteers either exercised on recumbent ergometer at 75 % V 4 O 2 max for 60 min (exercise session) or sat quietly (resting session). Saliva samples were obtained at 60 min intervals during sessions for measurements of salivary stress markers (cortisol, IgA and CgA), salivary inflammatory cytokines, such as interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) and osmolality. Saliva flow rate was decreased and saliva osmolality was increased during the 60-min exercise. Saliva cortisol and CgA concentrations and secretion rates were increased during and after the exercise, whereas saliva IgA concentration and secretion rates were decreased after the exercise. Salivary inflammatory cytokines was increased during and after the exercise. The present findings suggested a single bout of prolonged strenuous exercise caused a transient increase in the salivary cortisol, CgA and inflammatory cytokines levels, whereas salivary IgA concentration and secretion rates were decreased after the exercise. Further studies, however, are needed to delineate whether or not salivary stress markers and inflammatory cytokines may be used as biological markers to determine the host responses to acute prolonged strenuous exercise.(Jpn. J. Phys. Fitness Sports Med., 60（ 3 ）: 295-304 (2011))

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“…2 A variety of inflammatory mediators including cytokines and chemokines are released by injured cells and infiltrating macrophages. 9,11 Although serum cytokine and chemokine response patterns to exercise of varying intensities [12][13][14][15] and multiple organ trauma and fractures have been studied, [16][17][18] exposure to more chronic, lower levels of injury are not yet well characterized.…”

mentioning

confidence: 99%

Serum and tissue cytokines and chemokines increase with repetitive upper extremity tasks

Barbe

Elliott

Abdelmagid

et al. 2008

Journal Orthopaedic Research

112

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We investigated inflammation in rats performing a low repetition, negligible force (LRNF) or high repetition, negligible force (HRNF) task of reaching and retrieving food pellets at target rates of two or four reaches/min for 2 h/day, for 6-8 weeks. Serum was assayed for 11 cytokines and chemokines; forelimb tissues for four cytokines. Macrophages were counted in forelimb tissues of LRNF rats to add to results from our previous studies of HRNF rats. In HRNF rats, serum IL-1a, IL-1b, TNFa, MIP2, MIP3a, and RANTES were elevated in weeks 6 and 8. In contrast, only MIP2 and MIP3a increased in serum of LRNF rats. In 8 week HRNF reach limb tissues, IL-1a, IL-1b, TNFa, and IL-10 increased in distal bones, IL-1a and -b in muscles, and TNFa in tendons. Only IL-10 increased in LRNF reach limb muscles in week 8. Serum IL-1a and MIP2 correlated with macrophages in LRNF loose connective tissues, serum MIP3a and MIP2 correlated negatively with grip strength, while serum TNFa, MIP3a, and MIP2 correlated positively with total number of reaches. Thus, several tissue and circulating cytokines/chemokines increase in an exposure dependent manner following short-term performance of repetitive reaching tasks and correlate with macrophage infiltration and decreasing grip strength. Keywords: cytokines; chemokines; macrophages; repetitive motion injury; WMSD Repetitive motion injuries (RMI) of the wrist and hand are painful, potentially disabling, and costly. Recent work suggests that RMIs induce injury in several tissue types in animal models, 1-6 as well as an early inflammatory response at the tissue level. 2,3,[7][8][9] Increases in four circulating inflammatory mediators, C-reactive protein, interleukin 1 beta (IL-1b), IL-6, and tumor necrosis factor alpha (TNFa) have also been shown to increase in patients with upper extremity overuse disorders. 10 The factors triggering underlying pathophysiological responses are still under investigation, which impedes progress toward their primary and secondary prevention.Using a rat model, we have reported that repetitive reaching causes injury and wide-spread increases in macrophage influx into musculotendinous tissues and peripheral nerves, extraneural fibrosis, decreased nerve conduction, and decreased grip strength. [2][3][4]7,9 The macrophage response is associated with increased inflammatory cytokines in the median nerve, 9 and increased serum IL-1a following HRNF task performance. 2 A variety of inflammatory mediators including cytokines and chemokines are released by injured cells and infiltrating macrophages. 9,11 Although serum cytokine and chemokine response patterns to exercise of varying intensities 12-15 and multiple organ trauma and fractures have been studied, [16][17][18] exposure to more chronic, lower levels of injury are not yet well characterized.Here, we examine several cytokines and chemokines in forelimb musculoskeletal tissues and serum to identify their response profiles, as well as potential cellular sources, after the performance of a voluntary repetitive ...

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Pro‐ and anti‐inflammatory cytokine balance in strenuous exercise in humans

Cited by 840 publications

References 22 publications

Serum from exercising humans suppresses t-cell cytokine production

Serum from exercising humans suppresses t-cell cytokine production

Effects of Acute Prolonged Strenuous Exercise on the Salivary Stress Markers and Inflammatory Cytokines

Serum and tissue cytokines and chemokines increase with repetitive upper extremity tasks

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