Applied Psychoneuro-immunology (PNI)

This online learning describes Psychoneuroimmunology (PNI), which is the study of the interaction between psychological processes and the nervous and immune systems of the human body.  PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, genetics and pharmacology.  The course also discusses the history/origin of PNI, the immune-brain loop and understanding stress and immune function.

How do stressful events and negative emotions influence the immune system, and how big are the effects? New multidisciplinary permutations provide fresh vistas and emphasize the importance of training psychologists more broadly so that they will be central and essential players in the advancement of biomedical science.

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In this on-line course, we use a PNI lens to understand and describe the complex influences of biology and psychology on inflammation.  Inflammation is an underlying etiological factor in many chronic diseases.  

A brief description of brain-immune communication is first introduced as background, followed by a summary of inflammation's effect on health.  The biological, psychological, and psychosocial influences on inflammation are then discussed, followed by a review of inflammation and cellular aging.

The increased morbidity and mortality associated with depression is substantial. In this paper, we review evidence suggesting that depression contributes to disease and death through immune dysregulation. This review focuses on recent human studies addressing the impact of depression on immune function, and the health consequences of those changes. There is growing evidence that depression can directly stimulate the production of proinflammatory cytokines that influence a spectrum of conditions associated with aging, including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, certain cancers, periodontal disease, frailty, and functional decline. 

Additionally, depression can down-regulate the cellular immune response; as a consequence, processes such as prolonged infection and delayed wound healing that fuel sustained proinflammatory cytokine production may be promoted by depression. These direct and indirect processes pose the greatest health risks for older adults who already show age-related increases in proinflammatory cytokine production. Thus, aging interacts with depression to enhance risks for morbidity and mortality.

Chronic stress is typically associated with suppression of the immune system, including impaired responses to infectious disease and delayed wound healing.  Recent work suggests that stress and depression can enhance production of proinflammatory cytokines, substances that regulate the body’s immune response to infection and injury. We provide a broad framework relating stress and depression to a range of diseases whose onset and course may be influenced by proinflammatory cytokines, particularly the cytokine interleukin-6 (IL-6).  IL-6 has been linked to a spectrum of chronic diseases associated with aging. Production of proinflammatory cytokines that influence these, and other conditions can be directly stimulated by chronic stress and depression.  

We suggest that a key pathway through which chronic stress and depression influence health outcomes involves proinflammatory cytokines. We discuss the evidence for relationships between psychosocial factors and proinflammatory cytokines, and important health implications of these findings.