These alterations in immune cells have been shown to Sorafenib Raf-1 correspond with the release of catecholamines [34]. In addition, our laboratory recently found that following a combined physical and psychological stress, NE area-under-the-curve (AUC) was negatively correlated with the percentage of CD19+ B cells, and heart rate (HR) was negatively associated with the percentage change in the CD4/CD8 ratio [35]. These elevations in NE and HR simultaneously in response to the dual challenge suggest greater sympathetic activation that, in turn, could possibly explain the alteration in the distribution of lymphocyte subsets, resulting in ineffective cell-mediated immune responses [36, 37]. Therefore, these findings indicate that acute stress enhances innate immunity and possibly suppresses adaptive immunity, and these alterations can be likely enhanced at higher intensities of physical stress.

The appropriate redistribution of immune cells in response to acute stressors is imperative to an effective and efficient immune response in preparation for potential invaders and injury [26, 38]. However, when exposed to chronic stress, immunoprotection can be suppressed by reducing immune cell number, function (cytotoxicity), and proliferation, thereby promoting susceptibility to diseases [39, 40]. Obesity is considered a chronic inflammatory condition that enhances the risk of numerous inflammatory diseases, including diabetes and cardiovascular disease (CVD). These obesity-attributable illnesses have been discovered to have a strong association with inflammatory parameters in plasma such as proinflammatory cytokines (TNF-�� and IL-6) [41, 42].

In addition to plasma inflammatory mediators, the circulating mononuclear cells in obese individuals may be more readily stimulated to produce inflammatory cytokines [43]. Interestingly, along with physical illnesses, obesity is associated with job-associated stress and psychosocial disorders such as depression and chronic anxiety [44�C46]. These stress-related disorders have been found to lead to increased risk of CVD and mortality in obese patients [47].Chronic stress has been shown to be associated with disturbances of the HA and SA axes and is linked to abdominal adiposity [48]. In response to acute stress, elevated cortisol levels are associated with high central adiposity [49�C51].

Furthermore, studies have demonstrated an increase in SA axis reactivity in obesity patients [52�C54]. This occurrence seems to be pivotal to understand how stress may upregulate the inflammatory conditions in obese individuals. Recently, studies have shown that obese subjects exhibit higher proinflammatory cytokine production such as IL-6 in plasma and ex vivo compared with Dacomitinib normal-weight subjects in response to acute mental stress [50, 55].