Stress, chronic inflammation, and emotional and physical well-being: concurrent effects and chronic sequelae.

The importance of T(H) cells (specifically T(H)2 cells) that produce IL-4, -5, -10, and -13 in the propagation of chronic allergic inflammation is well known. However, the role of the hypothalamic-pituitary-adrenal axis and the sympathetic system as immunomodulators of events leading to inflammation is less well established. Increases in stress levels are associated with elevations in circulating glucocorticoids and catecholamines, which may influence disease pathophysiologic factors and severity through changes in the number and activity of T(H)-cell populations and through other means. For instance, stress has been shown to shift the relative proportion and trafficking of T(H)1 and T(H)2 cells to a T(H)2 phenotype. In this article, the current understanding of interactions of the stress and immune systems and the physiologic and pathophysiologic implications of these interactions in human health and disease are reviewed.