Respiratory infection risk in athletes: association with antigen-stimulated IL-10 production and salivary IgA secretion.
ABSTRACT The purpose of this study was to examine factors influencing susceptibility to upper respiratory tract infections (URTI) in 18-35-year-old men and women engaged in endurance-based physical activity during the winter months. Eighty individuals (46 males, 34 females) provided resting blood and saliva samples for determination of markers of systemic immunity. Weekly training and illness logs were kept for the following 4 months. Thirty subjects did not experience an URTI episode and 24 subjects experienced 3 or more weeks of URTI symptoms. These illness-prone subjects had higher training loads and had ∼2.5-fold higher interleukin (IL)-4 and IL-10 production by antigen-stimulated whole blood culture than the illness-free subjects. Illness-prone subjects also had significantly lower saliva S-IgA secretion rate and higher plasma IgM (but not IgA or IgG) concentration than the illness-free subjects. There were no differences in circulating numbers of leukocyte subtypes or lymphocyte subsets between the illness-prone and illness-free subjects. The production of IL-10 was positively correlated and the S-IgA secretion rate was negatively correlated with the number of weeks with infection symptoms. It is concluded that high IL-10 production in response to antigen challenge and low S-IgA secretion are risk factors for development of URTI in physically active individuals.
- SourceAvailable from: Elena Papacosta[Show abstract] [Hide abstract]
ABSTRACT: Although resting immune function is not very different in athletes compared with non-athletes periods of intensified training (overreaching) in already well trained athletes can result in a depression of immunity in the resting state. Illness-prone athletes appear to have an altered cytokine response to antigen stimulation and exercise. Having low levels of salivary IgA secretion also makes athletes more susceptible to upper respiratory tract infections. Overtraining is associated with recurrent infections and immunodepression is common, but immune functions do not seem to be reliable markers of impending overtraining. There are several possible causes of the diminution of immune function associated with periods of heavy training. One mechanism may simply be the cumulative effects of repeated bouts of intense exercise (with or without tissue damage) with the consequent elevation of stress hormones, particularly glucocorticoids such as cortisol, causing temporary inhibition of TH-1 cytokines with a relative dampening of the cell-mediated response. When exercise is repeated frequently there may not be sufficient time for the immune system to recover fully. Tapering has been described as a gradual reduction in the training load which allows the recovery of physiological capacities that were impaired by previous intensive training and permits further training-induced adaptations to occur accompanied by competition performance enhancements. The majority of the studies that have examined the recovery of immunoendocrine responses during 1-3 week tapers in trained athletes have mainly reported enhanced performance, often accompanied by increased anabolic activity, reduced physiological stress and restoration of mucosal immunity and immune function.Revista Brasileira de Educação Física e Esporte. 03/2013; 27(1):159-176.
- [Show abstract] [Hide abstract]
ABSTRACT: Glucose and glutamine are important energetic and biosynthetic nutrients for T and B lymphocytes. These cells consume both nutrients at high rates in a function-dependent manner. In other words, the pathways that control lymphocyte function and survival directly control the glucose and glutamine metabolic pathways. Therefore, lymphocytes in different functional states reprogram their glucose and glutamine metabolism to balance their requirement for ATP and macromolecule production. The tight association between metabolism and function in these cells was suggested to introduce the possibility of several pathologies resulting from the inability of lymphocytes to meet their nutrient demands under a given condition. In fact, disruptions in lymphocyte metabolism and function have been observed in different inflammatory, metabolic, and autoimmune pathologies. Regular physical exercise and physical activity offer protection against several chronic pathologies, and this benefit has been associated with the anti-inflammatory and immunomodulatory effects of exercise/physical activity. Chronic exercise induces changes in lymphocyte functionality and substrate metabolism. In the present review, we discuss whether the beneficial effects of exercise on lymphocyte function in health and disease are associated with modulation of the glucose and glutamine metabolic pathways.Mediators of Inflammation 01/2014; 2014:326803. · 3.88 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Background Obesity is a severe health problem worldwide which leads to multiple comorbidities including type 2 diabetes mellitus and cardiovascular diseases. Inflammation has been found to be an important characteristic of adipose tissue in obese subjects. However, obesity is also associated with compromised immune responses to infections and the impact of obesity on immune function has not been fully understood.Subjects/Methods To clarify the role of obesity in the immune responses, we investigated the Toll-like receptor (TLR)-induced cytokine secretion by leukocytes from obese and lean subjects. We also investigated the relationship between insulin-induced intracellular signaling and cytokine production using peripheral blood mononuclear cells (PBMC) and a monocytic cell line THP-1.ResultsWe found decreased TLR-induced interferon-gamma (IFN-γ), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) secretions and elevated IL-10 secretion by leukocytes from obese subjects when compared with lean controls. PBMCs from obese subjects showed enhanced basal Akt and glycogen synthase kinase 3β (GSK-3β) phosphorylation which did not further increase with insulin and lipopolysaccharide (LPS) stimulation. We also found that LPS-induced IκBα degradation was inhibited in PBMCs from obese subjects. By using THP-1 cells with GSK-3β knockdown or cells treated with hyperinsulinemic and high fatty acid conditions, we found that LPS-induced NF-κB activation was inhibited and cAMP response element-binding protein (CREB) activation was enhanced.Conclusions These findings indicate that GSK-3β is important in the regulation of NF-κB and CREB activation in leukocytes under the metabolic condition of obesity. Our study revealed a key mechanism through which metabolic abnormalities compromise leukocyte functions in people with obesity.International Journal of Obesity accepted article preview online, 23 May 2014; doi:10.1038/ijo.2014.93.International journal of obesity (2005) 05/2014; · 5.22 Impact Factor