β-Endorphin and natural killer cell cytolytic activity during prolonged exercise. Is there a connection?

Gannon, G. A.; Rhind, Shawn G.; Suzui, Masatoshi; Zámečník, Jiří; Sabiston, Brian H.; Shek, Pang N.; Shephard, Roy J.

doi:10.1152/ajpregu.1998.275.6.r1725

Cited by 12 publications

(15 citation statements)

References 48 publications

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“…Various authors observed stimulatory and inhibitory effects mainly on mixed cell fraction [4]. For example, the production of γ-IFN was suppressed by a mechanism realized through µ-receptor on monocytes and stimulated through a nonopioid receptor.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of the Effect of β-Endorphin on IL-4 and γ-IFN Production by CD4+ Lymphocytes

Гейн

Gorshkova

2008

Bull Exp Biol Med

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Beta-endorphin stimulates phytohemagglutinin-induced production of IL-4 and does not modify the production of gamma-IFN in nonfractionated leukocyte suspension. In a culture of purified CD4+ T-cells, beta-endorphin does not modify the levels of IL-4 and gamma-IFN, but stimulates the production of IL-4 and inhibits gamma-IFN production after addition of monocytes to CD4+ lymphocytes. Stimulation of IL-4 synthesis by beta-endorphin is mediated by the cycloxygenase cycle products. Hence, beta-endorphin shifts T-helper polarization towards Th2 cells with subsequent predominance of the humoral form of the immune response.

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Section: Resultsmentioning

confidence: 99%

Evaluation of the Effect of β-Endorphin on IL-4 and γ-IFN Production by CD4+ Lymphocytes

Гейн

Gorshkova

2008

Bull Exp Biol Med

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“…A double blind randomised block trial used oral naloxone to counter -endorphin, 61 and indomethacin to counter prostaglandin release. 62 The -endorphin antagonist had no eVect other than to reduce the exercise induced increment of -endorphin, but prostaglandin levels did increase during vigorous aerobic activity.…”

Section: Effect Of Anti-inflammatory Agents and Endorphin Antagonistsmentioning

confidence: 99%

Sepsis and mechanisms of inflammatory response: is exercise a good model?

Shephard¹

2001

Br J Sports Med

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Objectives-The immune changes induced by a bout of prolonged and vigorous exercise have been suggested to be a useful experimental model of sepsis and the inflammatory response. Available literature was reviewed to evaluate this hypothesis. Methods-Literature describing the immune response to various patterns of exercise was compared with data on the immune changes observed during sepsis and inflammation. Results-Although there are qualitative similarities between the immune responses to exercise and sepsis, the magnitude of the changes induced by most forms of exercise remains much smaller than in a typical inflammatory response. Indeed, the exercise induced changes in some key elements such as plasma cytokine concentrations are too small to be detected reliably by current technology. Conclusions-If exercise is to provide a valid model of sepsis and the inflammatory response, it will be necessary to focus on subjects who are willing to exercise extremely hard, to use the pattern of exercise that has the greatest eVect on the immune system, and to combine this stimulus with other psychological, environmental, or nutritional stressors. (Br J Sports Med 2001;35:223-230)

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“…1999). Surface density of CD2 on CD56+ NK cells has also been shown to decrease after prolonged, low intensity exercise (Gannon et al . 1998).…”

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confidence: 99%

The relationship of natural killer cell counts, perforin mRNA and CD2 expression to post‐exercise natural killer cell activity in humans

Miles

Mackinnon

Grove

et al. 2002

Acta Physiologica Scandinavica

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The aim of this study was to further investigate the mechanism of suppression of natural killer (NK) cell cytotoxic activity in peripheral blood following strenuous exercise. Blood was collected for analysis of NK cell concentration, cytotoxic activity, CD2 surface expression and perforin gene expression from runners (RUN, n=6) and resting controls (CONTROL, n=4) pre-exercise, 0, 1.5, 5, and 24 h following a 60-min treadmill run at 80% of VO2 peak. Natural killer cytotoxic activity, measured using a whole blood chromium release assay, fluctuated minimally in the CONTROL group and increased by 63% and decreased by 43% 0 and 1.5 h post-exercise, respectively, in the RUN group (group x time, P < 0.001). Lytic index (cytotoxic activity per cell) did not change. Perforin mRNA, measured using quantitative real-time polymerase chain reaction (QRT-PCR) decreased from pre- to post-exercise and remained decreased through 24 h. The decrease from pre- to 0 h post-exercise was seen predominately in the RUN group and was inversely correlated (r=- 0.95) to pre-exercise perforin mRNA. The NK cell surface expression of CD2 (lymphocyte function-associated antigen-2) was determined using fluorescent antibodies and flow cytometry. There was no change in the proportion of NK cells expressing CD2 or CD2 density. We conclude that (1) numerical redistribution accounted for most of the change in NK cytotoxic activity following a strenuous run, (2) decrease in perforin gene expression during the run was inversely related to pre-exercise levels but did not parallel changes in cytotoxic activity, and (3) CD2 surface expression was not affected by exercise.

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β-Endorphin and natural killer cell cytolytic activity during prolonged exercise. Is there a connection?

Cited by 12 publications

References 48 publications

Evaluation of the Effect of β-Endorphin on IL-4 and γ-IFN Production by CD4+ Lymphocytes

Evaluation of the Effect of β-Endorphin on IL-4 and γ-IFN Production by CD4+ Lymphocytes

Sepsis and mechanisms of inflammatory response: is exercise a good model?

The relationship of natural killer cell counts, perforin mRNA and CD2 expression to post‐exercise natural killer cell activity in humans

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