Exercise Immunology Review最新文献

The T-cell subset Th17 is induced partly by interleukin (IL)-6 and activated by IL-23, and produces a proinflammatory cytokine IL-17. Since IL-6 increases dramatically following long-lasting endurance exercise, this response may also stimulate the induction of IL-17 and IL-23 after exercise. The aim of this study was to clarify the dynamics of IL-17 in association with endurance exercise-induced muscle damage and inflammatory responses. Fourteen male triathletes participated in a duathlon race consisting of 5 km of running, 40 km of cycling and 5 km of running. Venous blood and urine samples were collected before, immediately after 1.5 h and 3 h after the race. Plasma and urine were analyzed using enzyme-linked immunosorbent assays (ELISA). Haematological and biochemical variables such as neutrophil activation marker (myeloperoxidase: MPO), muscle damage marker (myoglobin: Mb) and soluble receptor activator of nuclear factor (NF)-KB ligand (sRANKL) were also determined to estimate the biological and pathological significance. Plasma concentrations oflL-6 (+26.0x), MPO (+3.2x) and Mb (+4.9x) increased significantly immediately after the race and IL-17 and IL-23 tended to increase. Furthermore, plasma concentrations of IL-12p40 and sRANKL increased significantly after the race. The measured parameters related to Thl 7 cytokines in the urinary output were closely correlated with each other and muscle damage marker. These findings suggest that IL-17 induced by IL-6 and activated by IL-23 or other IL-17 producing-cells and IL-23 might promote neutrophil activation and muscle damage following prolonged endurance exercise.

Type 1 (TI) and Type 2 (T2) lymphocytes promote cell-mediated immunity and humoral immunity respectively. Evidence accumulated over the past two decades has demonstrated diverse responses of T1 and T2 cells to acute exercise or long-term training at moderate and high intensities. This brief review highlights the current findings from animal and human experimental models on the relationship between the T1 and T2 cell counts and the cytokines these cells produce, in response to moderate and high intensity exercise. The potential of using the T1/T2 balance as an indicator of immune function changes in response to exercise is discussed.

Exercise can alter human health in both beneficial (e. g. reduced risk of infection and of atherosclerosis) and adverse (e. g. anaphylaxis, exercise-induced asthma, and exacerbation of chronic illness) ways. Hitherto, the mechanisms linking exercise and health are not fully understood, but may rest on the capability of exercise to both increase circulating immune cells and modulate their activity. Natural killer (NK) cells, a major component of innate immunity, are one of the most sensitive populations of immune cells to exercise stress. NK cells play an important role in the detection and elimination of tumours and virus-infected cells. To mediate NK cell functions, there is an array of activating and inhibitory receptors with distinct specificities on their surface. Killer-cell immunoglobulin-like receptors (KIRs) which bind to MHC class I are a key example of receptors expressed by NK cells. The combination of MHC class I and KIR variants influences resistance to infections, susceptibility to autoimmune diseases, as well as complications of pregnancy. It is suggested that KIRs may also determine a considerable part of the effects of physical activity on human health. In this review we discuss KIRs in more detail, their role in the onset of human diseases, and the influence of acute exercise on KIR gene expression.

An ever-growing volume of peer-reviewed publications speaks to the recent and rapid growth in both scope and understanding of exercise immunology. Indeed, more than 95% of all peer-reviewed publications in exercise immunology (currently >2, 200 publications using search terms "exercise" and "immune") have been published since the formation of the International Society of Exercise and Immunology (ISEI) in 1989 (ISI Web of Knowledge). We recognise the epidemiological distinction between the generic term "physical activity" and the specific category of "exercise", which implies activity for a specific purpose such as improvement of physical condition or competition. Extreme physical activity of any type may have implications for the immune system. However, because of its emotive component, exercise is likely to have a larger effect, and to date the great majority of our knowledge on this subject comes from exercise studies.

When menstrual phase and oral contraceptives are controlled for, males and females display marked differences in immune response to an exercise stress. In highly controlled research studies, sex differences in immune cell changes, cytokine alterations, along with morbidity and mortality after inoculation are apparent. Exercise has been hypothesized to serve as a model of various clinical stresses by inducing similar hormonal and immunological alterations. Thus, a greater understanding of sex differences in post exercise non-specific immune function may provide insight into more effective clinical approaches and treatments. This paper reviews the recent evidence supporting sex differences in post exercise immune response and highlights the need for greater control when comparing the post exercise immune response between sexes.

The physical training undertaken by athletes is one of a set of lifestyle or behavioural factors that can influence immune function, health and ultimately exercise performance. Others factors including potential exposure to pathogens, health status, lifestyle behaviours, sleep and recovery, nutrition and psychosocial issues, need to be considered alongside the physical demands of an athlete's training programme. The general consensus on managing training to maintain immune health is to start with a programme of low to moderate volume and intensity; employ a gradual and periodised increase in training volumes and loads; add variety to limit training monotony and stress; avoid excessively heavy training loads that could lead to exhaustion, illness or injury; include non-specific cross-training to offset staleness; ensure sufficient rest and recovery; and instigate a testing programme for identifying signs of performance deterioration and manifestations of physical stress. Inter-individual variability in immunocompetence, recovery, exercise capacity, non-training stress factors, and stress tolerance likely explains the different vulnerability of athletes to illness. Most athletes should be able to train with high loads provided their programme includes strategies devised to control the overall strain and stress. Athletes, coaches and medical personnel should be alert to periods of increased risk of illness (e.g. intensive training weeks, the taper period prior to competition, and during competition) and pay particular attention to recovery and nutritional strategies.

The endolysosome pathway has been proposed for secretion of heat shock protein (Hsp)72 with a regulatory role for extracellular adenosine triphosphate (ATP). Here, we tested the hypothesis that extracellular ATP mediates the increase in plasma Hsp72 after exercise. We measured plasma ATP Hsp72, cathepsin D, norepinephrine, free fatty acid, glucose, and myoglobin in 8 healthy young males (mean +/- SE: age, 22.3 +/- 0.3 years; height, 171.4 +/- 0.8 cm; weight, 68.8 +/- 3.1 kg; body mass index, 23.5 +/- 1.1 kg/cm2; VO2 max, 44.1 +/- 3.8 mL/kg/min) before and at 0, 10, 30, and 60 min after aerobic exercise (cycling) and elbow flexor eccentric exercise. Subjects cycled for 60 min at 70-75% VO2 max (mean +/- SE; 157.4 +/- 6.9 W). Eccentric strength exercise consisted of flexing the elbow joint to 90 degrees with motion speed set at 30 degrees/sec at extension and 10 degrees/sec at flexion. Subjects performed 7 sets of 10 eccentric actions with a set interval of 60 sec. The motion range of the elbow joint was 90 degrees-180 degrees. Compared with the levels of Hsp72 and ATP in plasma after bicycle exercise, those after eccentric exercise did not change. A significant group x time interaction was not observed for Hsp72 or ATP in plasma. A significant correlation was found between Hsp72 and ATP in plasma (r=0.79, P<0.05), but not between Hsp72 and norepinephrine (r=0.64, P=0.09) after bicycle exercise. A significant correlation between ATP and norepinephrine in plasma was found (r=0.89 P<0.01). We used stepwise multiple-regression analysis to determine independent predictors of exercise-induced elevation of eHsp72. Candidate predictor variables for the stepwise multiple-regression analysis were time (Pre, Post, Post10, Post30, Post60), exercise type (aerobic, eccentric), ATP, cathepsin D, norepinephrine, epinephrine, glucose, and FFA. In the regression model for Hsp72 in plasma, increased ATP and glucose were the strongest predictors of increased Hsp72 (ATP: R2=0.213, beta=0.473, P=0.000; ATP and glucose: R2=0.263, beta=0.534, P=0.000). Collectively, these results imply that ATP in plasma is a trigger of Hsp72 release after exercise.

The purpose of this study was to examine sex differences in immune variables and upper respiratory tract infection (URTI) incidence in 18-35 year-old athletes engaged in endurance-based physical activity during the winter months. Eighty physically active individuals (46 males, 34 females) provided resting venous blood samples for determination of differential leukocyte counts, lymphocyte subsets and whole blood culture multi-antigen stimulated cytokine production. Timed collections of unstimulated saliva were also made for determination of saliva flow rate, immunoglobulin A (IgA) concentration and IgA secretion rate. Weekly training and illness logs were kept for the following 4 months. Training loads averaged 10 h/week of moderate-vigorous physical activity and were not different for males and females. Saliva flow rates, IgA concentration and IgA secretion rates were significantly higher in males than females (all P < 0.01). Plasma IgA, IgG and IgM concentrations and total blood leukocyte, neutrophil, monocyte and lymphocyte counts were not different between the sexes but males had higher numbers of B cells (P < 0.05) and NK cells (P < 0.001). The production of interleukins 1 beta, 2, 4, 6, 8 and 10, interferon-gamma and tumour necrosis factor-alpha in response to multi-antigen challenge were not significantly different in males and females (all P > 0.05). The average number of weeks with URTI symptoms was 1.7 +/- 2.1 (mean +/- SD) in males and 2.3 +/- 2.5 in females (P = 0.311). It is concluded that most aspects of immunity are similar in men and women in an athletic population and that the observed differences in a few immune variables are not sufficient to substantially affect URTI incidence. Sex differences in immune function among athletes probably do not need to be considered in future mixed gender studies on exercise, infection and immune function unless the focus is on mucosal immunity or NK cells.

The 'open window' theory is characterised by short term suppression of the immune system following an acute bout of endurance exercise. This window of opportunity may allow for an increase in susceptibility to upper respiratory illness (URI). Many studies have indicated a decrease in immune function in response to exercise. However many studies do not indicate changes in immune function past 2 hours after the completion of exercise, consequently failing to determine whether these immune cells numbers, or importantly their function, return to resting levels before the start of another bout of exercise. Ten male 'A' grade cyclists (age 24.2 +/- 5.3 years; body mass 73.8 +/- 6.5 kg; VO2peak 65.9 +/- 7.1 mL x kg(-1) x min(-1)) exercised for two hours at 90% of their second ventilatory threshold. Blood samples were collected pre-, immediately post-, 2 hours, 4 hours, 6 hours, 8 hours, and 24 hours post-exercise. Immune variables examined included total leukocyte counts, neutrophil function (oxidative burst and phagocytic function), lymphocyte subset counts (CD4+, CD8+, and CD16+/56+), natural killer cell activity (NKCA), and NK phenotypes (CD56dimCD16+, and CD56(bright)CD16-). There was a significant increase in total lymphocyte numbers from pre-, to immediately post-exercise (p < 0.01), followed by a significant decrease at 2 hours post-exercise (p < 0.001). CD4+ T-cell counts significantly increased from pre-exercise, to 4 hours post- (p < 0.05), and 6 hours post-exercise (p < 0.01). However NK (CD16+/56+) cell numbers decreased significantly from pre-exercise to 4 h post-exercise (p < 0.05), to 6 h post-exercise (p < 0.05), and to 8 h post-exercise (p < 0.01O). In contrast, CD56(bright)CD16- NK cell counts significantly increased from pre-exercise to immediately post-exercise (p < 0.01). Neutrophil oxidative burst activity did not significantly change in response to exercise, while neutrophil cell counts significantly increased from pre-exercise, to immediately postexercise (p < 0.05), and 2 hours post-exercise (p < 0.01), and remained significantly above pre-exercise levels to 8 hours post-exercise (p < 0.01). Neutrophil phagocytic function significantly decreased from 2 hours post-exercise, to 6 hours post- (p < 0.05), and 24 hours post-exercise (p < 0.05). Finally, eosinophil cell counts significantly increased from 2 hours post to 6 hours post- (p < 0.05), and 8 hours post-exercise (p < 0.05). This is the first study to show changes in immunological variables up to 8 hours post-exercise, including significant NK cell suppression, NK cell phenotype changes, a significant increase in total lymphocyte counts, and a significant increase in eosinophil cell counts all at 8 hours post-exercise. Suppression of total lymphocyte counts, NK cell counts and neutrophil phagocytic function following exercise may be important in the increased rate of URI in response to regular intense endurance training.

Prolonged exhaustive exercise has a great impact on the immune system of athletes and leads to a transient weakening of the immune system. A host of studies has documented changes of immune parameters in peripheral blood following exercise. Concerning the effect of exhaustive exercise in transplant recipients there is little knowledge at present. We analysed peripheral blood in healthy athletes and transplant recipients who participated in the "Euregio cycling tour 2009" before and immediately after they performed 81 km of cycling that included ascending more than 1800 m in altitude. A full blood count and an automated differential count as well as microarray analysis were performed before, immediately after and one day after exercise in 10 male patients carrying a kidney transplant and in 10 controls matched in age and gender. Comparing the absolute increase in neutrophils in these two groups, we detected that the relative increase in neutrophils was significantly smaller in transplant recipients compared to their corresponding controls after exhaustive exercise. While both groups were comparable in performance, microarray analysis revealed a markedly different pattern of gene expression in transplant recipients compared to their controls. From the 130 genes that were significantly upregulated in controls immediately after exercise, only 12 genes were also upregulated in transplant recipients. 64 different genes were upregulated in transplant recipients only. Our findings may be related to the immunosuppressive medication that the transplant recipients took and therefore it should also be discussed that regular exercise might reduce the need for immunosuppressive medication in transplant recipients.