Latent Cytomegalovirus infection amplifies CD8 T-lymphocyte mobilisation and egress in response to exercise

Abstract

Exercise induces mobilisation of CD8+ T lymphocytes (CD8TL) into the peripheral blood. This response is largely confined to effector-memory CD8TLs: antigen experienced cells which have a strong tissue-homing and effector potential. This study investigated whether effector-memory cells also account for the CD8TL egress from peripheral blood following exercise. As latent Cytomegalovirus (CMV) infection is associated with a robust expansion in the number and proportion of effector-memory CD8TLs, we also investigated if CMV serostatus was a determinant of the CD8TL responses to exercise. Fourteen males (Mean age 35, SD ± 14 yrs), half of whom were CMV seropositive (CMV+), ran on a treadmill for 60 min at 80% V_ O2 max. Blood was collected at baseline, during the final minute of exercise, and 15 min and 60 min thereafter. CD8TL memory subsets were characterised by flow cytometry, using the cell-surface markers CD45RA, CD27, and CD28. The results confirmed that CD8TLswith an effector-memory phenotype (CD27CD28CD45RA+/) exhibited the largest increase during exercise (+200% to +250%), and also showed the largest egress from blood 60 min post-exercise (down to 40% of baseline values). Strikingly, the mobilisation and subsequent egress of total CD8TLs was nearly twice as large in CMV+ individuals. This effect appeared specific to CD8TLs, and was not seen for CD4+ T lymphocytes or total lymphocytes. This effect of CMV serostatus was largely driven by the higher numbers of exercise-responsive effector-memory CD8TLs in the CMV+ participants. This is the first study to demonstrate that infection history is a determinant of immune system responses to exercise

Effect of acute and regular exercise on growth hormone secretagogue receptor-1a expression in human lymphocytes, T cell subpopulation and monocytes

“…These recruited cells appear also to be those with potent effector/cytotoxic functions whereas those that preferentially transmigrate into the tissues have tissue migratory phenotypes (Simpson et al, 2008;Turner et al, 2010). In this way there appears to be a selective deployment of specific cell subpopulations that are deemed most able to respond effectively to an immune/inflammatory challenge (Dhabhar, 2009).…”

Exercise-induced B cell mobilisation: Preliminary evidence for an influx of immature cells into the bloodstream

“…The primary mechanism for this effect is the expression of β2-adrenergic receptors on the surface of lymphocytes [10], that, in response to exerciseinduced elevations in catecholamine levels, induce lymphocyte detachment from the vascular endothelium and subsequent lymphocyte release into the peripheral bloodstream [2,34]. The most exerciseresponsive lymphocyte populations (with the highest β2-adrenergic receptor expression density) are natural killer (NK) cells and effector memory CD8+ T cells [3,4,43]. These populations are capable of mounting rapid effector functions that may bolster immune competence [3].…”

The BASES Expert Statement on Exercise, Immunity, and Infection

“…For example, it has been shown that symptoms of URTI in swimmers were positively associated with previous Epstein-Barr viral infection and partially with viral shedding (Gleeson et al, 2002). Furthermore, there is increasing evidence that infection history has a strong influence on cellular immune responses to exercise (Turner et al, 2010;Simpson et al, 2011).…”