Infection

Abstract

Stress, both physiological and psychological, plays an important role in altering susceptibility to infectious diseases caused by microorganisms such as bacteria and viruses. This review summarizes some of the newer information developed in the past few decades concerning the nature and mechanism of stress-associated infectious diseases. Various stressors increase the susceptibility of experimental animals to microbial infection. One of the most important factors is an increase of stress-enhanced glucocorticoids, decreasing humoral and cellular immune responses and increasing susceptibility to opportunistic microorganisms that normally are not pathogenic in nonstressed individuals. Many animal models show that increased corticosteroid levels are associated with stress and increased susceptibility to challenge infection with bacteria or viruses. Physiological studies with patients also show increased glucocorticoid levels associated with stress, either for physical or psychological reasons. This results in stress-induced immunomodulatory hormones, paralleling increased susceptibility to infection. The interrelationship between the nervous and immune systems is complex, and stress conditions increase susceptibility to many infectious microorganisms, as evidenced by the strong modulation of the immune response system by a wide variety of central nervous system-derived neuropeptides and hormones. Stress is a major factor in the progression of many infectious diseases in humans as well as in experimental and domestic animals. Stress-induced immune dysregulation involves complex interactions among the central nervous, endocrine, and immune systems. Ongoing and future studies, including those in neurobiology, immunology, and microbiology, will undoubtedly provide an even better understanding of the role of stress in infectious diseases.