Exercise Immunology Review最新文献

An increasing number of studies have examined how the immune system of patients with Chronic Fatigue Syndrome (CFS), or myalgic encephalomyelitis, responds to exercise. The objective of the present study was to systematically review the scientific literature addressing exercise-induced immunological changes in CFS patients compared to healthy control subjects. A systematic literature search was conducted in the PubMed and Web of science databases using different keyword combinations. We included 23 case control studies that examined whether CFS patients, compared to healthy sedentary controls, have a different immune response to exercise. The included articles were evaluated on their methodological quality. Compared to the normal response of the immune system to exercise as seen in healthy subjects, patients with CFS have a more pronounced response in the complement system (i.e. C4a split product levels), oxidative stress system (i.e. enhanced oxidative stress combined with a delayed and reduced anti-oxidant response), and an alteration in the immune cells' gene expression profile (increases in post-exercise interleukin-10 and toll-like receptor 4 gene expression), but not in circulating pro- or anti-inflammatory cytokines. Many of these immune changes relate to post-exertional malaise in CFS, a major characteristic of the illness. The literature review provides level B evidence for an altered immune response to exercise in patients with CFS.

It is widely recognized that exercise has an important role in inflammation regulation. To understand inflammatory mechanisms, extensive studies on the transcriptome and proteome have been conducted. However, interpreting these results is difficult, partly due to technical difficulties that impose some restriction on the accuracy and comprehensiveness of measurements. Here we first mention some limitations of studies involving large scale proteomics and high-throughput transcriptomics and further introduce a newly developed genome-wide translational analysis which may overcome some of the limitations and discover novel cellular dynamics. We then show preliminary results obtained by conducting a genome-wide translational analysis of the early inflammatory response of macrophages in response to lipopolysaccharide (LPS), and discuss the potential to identify novel factors by employing a genome-wide translational analysis.

Physical exercise is well known to affect leukocyte numbers and function. While regular exercise training has been shown to enhance specific immune functions, acute bouts of intensive exercise often lead to a pro-inflammatory response accompanied by a transient lymphocytopenia and neutrophilia. It can be assumed, that lymphocytopenia can be attributed at least partially to an enhanced lymphocyte apoptosis. In contrast, regulation of neutrophil apoptosis after exercise remains controversial since studies demonstrated both an up-regulation as well as a down-regulation of cell death. However, these discrepancies may be due to differences in exercise protocols, subjects' fitness levels, and to different methodological approaches. Two major signalling pathways of exercise induced apoptosis have been identified. First the external receptor mediated pathway using death receptors, and second the internal, oxidative-mediated pathway which encompasses the mitochondria. Potential apoptosis modulating mediators are reactive oxygen species (ROS), glucocorticoids and cytokines which are part of the systemic inflammatory response evoked after acute intensive exercise. Finally, the physiological impact and clinical relevance of leukocyte apoptosis will be discussed. On the one hand, exercise-induced apoptosis might be a mechanism to remove activated and potentially autoreactive immune cells. On the other hand, apoptosis might be a regulatory mechanism which is necessary for tissue reorganization and adaptational training processes.

A large body of evidence indicates modified expression of protein-coding genes in response to different kinds of physical activity. Recent years have exposed another level of regulation of cellular processes mediated by non-coding RNAs. MicroRNAs (miRNAs) are one of the largest families of non-coding RNAs. MiRNAs mediate post-transcriptional regulation of gene expression. The amount of data supporting the key role of miRNAs in the adaptation of the immune and other body systems to exercise steadily grows. MiRNAs change their expression profiles after exercise and seem to be involved in regulation of exercise-responsive genes in immune and other cell types. Here we discuss existing data and future directions in the field.

The purpose of this study was to examine sex differences in oral-respiratory mucosal immunity and the incidence, severity and duration of upper respiratory symptoms (URS) episodes in endurance athletes during a 16-week winter training period. Blood was collected from 210 subjects (147 men and 63 women) at the start and end of the study for determination of differential leukocyte counts. Timed collections of unstimulated saliva were obtained at the start and at 4-week intervals during the study period. Saliva samples were analysed for salivary antimicrobial peptides and proteins (AMPs). Weekly training and daily illness logs were kept using validated questionnaires. Training loads averaged 11 h/week of moderate-vigorous physical activity and were not different for males and females. The salivary concentration of lysozyme and lactoferrin (both P < 0.04) but not salivary immunoglobulin A (SIgA) or amylase were higher in males than females. Saliva flow rates were significantly higher in males than females (P < 0.03) and consequently so were the salivary secretion rates of lysozyme, lactoferrin and amylase (all P < 0.01) but not SIgA (P = 0.097). Total blood leukocyte, monocyte and lymphocyte counts were not different between the sexes but females had higher numbers of circulating neutrophils (P = 0.040). The average number of URS episodes was 0.6 +/- 0.8 (mean +/- SD) in males and 0.8 +/- 1.0 in females (P = 0.103) and the number of URS days was higher in females (4.7 vs 6.8 days, P < 0.02). The duration of URS episodes was longer in females (11.6 vs 15.5 days, P < 0.03). The findings of this study concur with recent reports of illness incidence at major competitive games indicating that female athletes may be more susceptible than their male counterparts to URS and that lower oral-respiratory mucosal immunity may, in part, account for this.

Salivary antimicrobial protein (AMP) expression is a primary determinant of mucosal immunity. This expression can be altered by exercise. While salivary IgA has been extensively studied, less is known about Lysozyme (Lys) and Lactoferrin (Lac). Knowledge on how sex and menstrual phase affect mucosal immunity is also limited. The purpose of this study was to examine how sex, menstrual phase, and exercise impact IgA, Lys, and Lac expression. Men (n = 9) and women (n = 9) ran for 45 min at 75% VO2(peak). Women were tested in the follicular and luteal phase. Saliva was collected pre-exercise, immediately post-exercise and 1 h postexercise. Pre-exercise, women had higher secretion rates of IgA compared to men (154 +/- 106 vs 85 +/- 44 microg/min) (p < 0.05). Lac secretion rate increased with exercise in both sexes and remained above baseline 1 h after exercise in men (7460 +/- 4839 ng/min), but had returned to pre-exercise levels at 1 h post-exercise in women (5720 +/- 4661 ng/min) (time * sex interaction, p < 0.05). Men had higher secretion rates of Lys (p < 0.05) at each time point compared to women (Men pre-exercise: 31042 +/- 23132, post-exercise: 29521 +/- 13205, 1 h post-exercise: 41229 +/- 31270 ng/min vs Women pre-exercise: 11585 +/- 10367, post-exercise: 22719 +/- 19452, 1 h post-exercise: 17303 +/- 11419 ng/min). Both sexes increased the secretion rate of Lys and Lac with exercise, whereas IgA was unchanged. Menstrual phase did not affect IgA, Lys, or Lac and men and women did not differ in saliva flow rates. In conclusion, regularly menstruating women who are not taking hormonal contraceptives differently express AMPs compared to men.

Plant alkaloids are found in foods, beverages, and supplements consumed by athletes for daily nutrition, performance enhancement, and immune function improvement. This paper examined possible immunomodulatory roles of alkaloids in exercise contexts, with a focus on human studies. Four representative groups were scrutinized: (a) caffeine (guaranine, mateine); (b) theophylline and its isomers, theobromine and paraxanthine; (c) ginger alkaloids including gingerols and shogaol; and (d) ephedra alkaloids such as ephedrine and pseudoephedrine. Emerging or prospective alkaloid sources (Goji berry, Noni berry, and bloodroot) were also considered. Human in vitro and in vivo studies on alkaloids and immune function were often conflicting. Caffeine may be immunomodulatory in vivo depending on subject characteristics, exercise characteristics, and immune parameters measured. Caffeine may exhibit antioxidant capacities. Ginger may exert in vivo anti-inflammatory effects in certain populations, but it is unclear whether these effects are due to alkaloids or other biochemicals. Evidence for an immunomodulatory role of alkaloids in energy drinks, cocoa, or ephedra products in vivo is weak to nonexistent. For alkaloid sources derived from plants, variability in the reviewed studies may be due to the presence of unrecognized alkaloids or non-alkaloid compounds (which may themselves be immunomodulatory), and pre-experimental factors such as agricultural or manufacturing differences. Athletes should not look to alkaloids or alkaloid-rich sources as a means of improving immune function given their inconsistent activities, safety concerns, and lack of commercial regulation.

A spinal cord injury (SCI) can increase the risk of infection by impacting on many aspects of immune function; one particularly well-documented observation is a reduction in lymphocyte numbers. The vast majority of lymphoid cells express adrenergic receptors. Therefore, autonomic function loss and concomitant alterations in resting and post-exercise catecholamine concentrations, particularly so in individuals with a tetraplegia, may impact directly on immune cells and depress immunity. Other factors are further likely to contribute, examples including altered muscular, endocrine and cardiovascular function following SCI. However, some alterations, such as increases in natural killer cell cytotoxicity following exercise in those with a tetraplegia, are unrelated to the catecholamine response. Likewise, mucosal immunity in individuals with a tetraplegia appears to be similarly influenced by exercise as in the able-bodied population. Indeed, rehabilitation therapy and exercise can increase some measures of immunity and autonomic function in those with an SCI. It is therefore possible that compensatory mechanisms offset disability-related detriments. This may be by way of sympathetic reflex activity, receptor hypersensitivity, or parasympathetic and neuroendocrine adjustments. Future work needs to explore these mechanisms further to clarify the implications of an SCI on the immune response to exercise and susceptibility to infection. In this article, we review the impacts of an SCI on immune, and specifically, exercise immune function. The relevant anatomical and physiological foundations of the immune system are first briefly laid out in order to understand the potential impacts of neural and neuroendocrine dysfunction on the immune system. With the limited number of human studies available, we have then aimed specifically to gather all relevant existing literature on exercise immunology in individuals with an SCI in patient, recreationally active and athlete populations. We believe that an understanding of the impacts of exercise can provide a tool to help maintain or improve health in individuals with an SCI. A comprehensive literature search was conducted using the search engines PubMed, SPORTDiscus, Web of Science and Zetoc, search period June 2012-February 2013. Key words employed included spinal cord injury, immunology, exercise, paraplegic, tetraplegic, upper body exercise, interleukin, immunoglobulin, sympathetic, and parasympathetic. All articles and articles derived from their reference lists were checked for their suitability.

Recently, many authors have proposed that mechanisms such as inflammation and/or allergies could be partly responsible for cases of upper respiratory tract illnesses that affect athletes after exhaustive exercise. Here we studied the kinetics of cytokines in the serum and nasal mucosa of athletes after a marathon. We were able to demonstrate an increase in serum levels of all interleukins studied immediately after the marathon in athletes that present or not with upper airways symptoms followed by a return to basal levels 72 hours after the race, as described in the literature. Interleukin (IL)-10 behaviour differed in the group of asymptomatic athletes. Measurement of this cytokine in protein extract of nasal mucosal cells showed increase 72 hours after the marathon. Levels of this cytokine in sera were increased at rest in athletes that did not present symptoms. These fin- dings suggest that the maintenance of a non-inflammatory environment in the mucosal airways is an active process that requires participation of the systemic and mucosal immune systems. We propose that the understanding of the upper airway disease of the athlete involves the study of mucosal and systemic immune systems.

The purpose of this study was to examine the influence of vitamin D status on mucosal and systemic immunity and the incidence, severity and duration of upper respiratory tract illness (URTI) episodes in endurance athletes during a 16-week winter training period. Blood was collected from 225 subjects at the start of the study and plasma was analysed for total 25-hydroxy vitamin D (25(OH)D) and cathelicidin concentration. Blood was also collected at the end of the study and analysed for 25(OH)D and antigen-stimulated cytokine production. Unstimulated saliva samples were obtained at the start and at 4-week intervals during the study period. Saliva samples were analysed for salivary antimicrobial peptides and proteins (AMPs). Weekly training and daily illness logs were kept. At the start and end of the study 38% and 55%, respectively, of the athlete cohort had inadequate (plasma 25(OH)D 30-50 nmol/L) or deficient (plasma 25(OH)D < 30 nmol/L) vitamin D status. There was a significantly higher proportion of subjects who presented with symptoms of URTI in the vitamin D deficient status group (initial plasma 25(OH)D < 30 nmol/L) during the study period than in the optimal vitamin D group (> 120 nmol/L) and the total number of URTI symptom days and the median symptom-severity score in the vitamin D deficient group was signifi- cantly higher than in the other groups. The plasma cathelicidin concentration positively correlated with the plasma 25(OH)D concentration and the saliva secretory immunoglobulin A (SIgA) secretion rate in the optimal vitamin D status group was significantly higher than in the other groups. Low vitamin D status was associated with lower pro-inflammatory cytokine production by monocytes and lymphocytes. Low vitamin D status could be an important determinant of URTI risk in endurance athletes and mucosal as well as systemic immunity may be modified via vitamin D-dependent mechanisms.