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Editor,—In assessing the health benefits and risks of physical activity, there has been much interest in the relation between exercise and the immune and inflammatory responses. However, only a very limited number of studies have examined the role of exercise on adhesion molecule profiles. P-selectin (CD62P) is an adhesion molecule expressed on activated platelets and endothelial cellsand is one of a group of related molecules that play an important role in leucocyte rolling on the vascular endothelium. Therefore it is intimately involved in the regulation of immune and inflammatory responses. Circulating forms of several adhesion molecules, including P-selectin, have been observed in humans, and elevated levels may reflect acute infection or inflammation. Alterations to the concentration of circulating adhesion molecules have also been associated with increased risk of specific diseases. High levels of soluble P-selectin, for example, have been associated with cardiovascular risk.1
My colleagues and I are interested in the influence of smoking on the aetiology of chronic inflammatory periodontal disease and have recently completed a study in which we observed the acute in vivo effect of smoking a standard 2R1 research cigarette on the serum concentration of a range of adhesion molecules and on adhesion molecule expression on circulating monocytes and neutrophils.2 As part of the experimental protocol, all subjects, who were apparently healthy, rested in a dental chair in a semi-reclined position for one hour. There were no statistically significant differences between the serum levels of soluble P-selectin of heavy smokers (n = 9; serum cotinine concentration≥100 ng/ml), light smokers (n = 10; serum cotinine concentration≤60 ng/ml), and non-smokers (n = 10; serum cotinine concentration≤10 ng/ml) at baseline. However, an incidental and unexpected observation was that soluble P-selectin concentrations fell significantly over the one hour rest period, independent of smoking status, as shown in fig 1.
It may be relevant to note that Kirkpatrick et al1 reported an increase in soluble P-selectin on repeated exercise in subjects with intermittent claudication. They concluded that the rise in soluble P-selectin after exercise may indicate progressive plateletactivation. Jilma et al3 had previously shown that, in healthy men, exercise could lead to an increase in the serum concentration of soluble intercellular adhesion molecule-1, another adhesion molecule involved in the chain of receptor-ligand interactions regulating leucocyte transmigration in inflammatory and immune responses.
We have shown that a period of rest can lead to a rapid decrease in circulating concentrations of soluble P-selectin. This observation is, to the best of our knowledge, entirely novel and may represent an important insight into the complex relation between physical activity and the inflammatory response. Further studies by those with expertise in sports physiology and medicine may be warranted.
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