Given the involvement of adipose tissue in the inflammatory process, especially namely in excessive states, it becomes an important clinical objective to identify lifestyle factors that may affect the obesity-immune system dynamic. For instance, stress, physical activity, and nutrition have each shown to be significant lifestyle factors influencing the inflammatory profile associated with the state of obesity [13�C15]. Of particular interest, it is well documented that chronic inflammation is also highly correlated to nutritional factors such as the type and amount of carbohydrates, proteins and fats that are consumed in the diet [16�C18]. Therefore, the purpose of this review is to comprehensively evaluate the impact of lifestyle factors, in particular psychological stress, physical activity, and nutrition, on obesity-related immune function with special focus on inflammation.

2. Stress and Obesity Stress in the body is established through some type of stressor(s), either physical or psychological. When stimulated, the human body responds in a complex manner, incorporating the intertwined activity of the endocrine and nervous systems (hypothalamic-pituitary-adrenal [HPA] and sympathoadrenal [SA] axes). Stress hormones such as cortisol from HPA axis and catecholamines (epinephrine (EPI) and norepinephrine (NE)) from the SA axis have been shown to alter immune cell responses, and this important immune system response coordinates a number of the body’s adaptations to the stressor.

Notably, elevations in stress hormones (cortisol and catecholamines) are thought to have detrimental effects on the immune system, leading to an imbalance between innate (immediate antigen-nonspecific defense) and adaptive immunity (specific response to a particular foreign antigen creating immunological memory) via the release of immune mediators such as cytokines [19]. In response to acute stress, the innate immune promptly prepares to provide immune protection followed by adaptive immunity when exposed to repeated or prolonged stress, whereas chronic stress can suppress these immune defenses. This stress-immune interaction is an important antiviral defense and fosters the elimination of invading microorganisms [20, 21].Research has shown that stress induces changes in immune cell distribution [22�C25], which ensures that the body’s immune response is efficient or elicits an effective immunoprotection.

An appropriate distribution of peripheral immune cells provides for the performance of surveillance and effector functions of the immune system [26]. The release of catecholamines and cortisol in response to stressors (physical GSK-3 or psychological) can mediate changes in the immune cell distribution [27, 28]. In response to acute stress, immune response is primarily regulated by catecholamines [24]. This is further supported by other studies demonstrating transient immune cell redistribution via beta-adrenergic activation following acute mental stress [23, 27, 29, 30].