Developmental Changes in the Neuroendocrine/Stress-Immune Interactions: Immunosenescence and Infectious/Inflammatory Disease Risk in the Elderly
In a recent review, Kathi Heffner from the Department of Psychiatry, University of Rochester Medical Center, Rochester, New York outlines recent data suggesting that immunosenescence, endocrinosenescence and age-related dysregulation of stress response systems are closely intertwined.
Immunosenescence refers to the dysfunction and gradual deterioration of the immune system associated with aging. This overall change in immunity contributes to the increased susceptibility of the elderly to infectious disease, cancer and pathological conditions relating to inflammation (e.g. cardiovascular disease, rheumatoid arthritis and possibly Alzheimer’s disease) and to the poor outcome of vaccination.
The natural age advancement is also accompanied by the aging and remodeling of the endocrine system – endocrinosenescence, and this process is closely related to immunosenescence, due to the immunomodulating properties of endocrine hormones. To add further complexity, aging and endocrinosenescence also affect the activity of the stress system in terms of stress hormones output, responsiveness and sensitivity of target tissues.
In the review, recently published in the Immunology and Allergy Clinics of North America, Dr. Heffner also highlights evidence indicating potentially additive or synergistic effects of immunosenescence and stress on immune and inflammatory dysregulation in older adults, further increasing disease risk.
The author of this review discusses that immunosenescence is characterized by two, inter-related changes in immunity. The first is related to chronic activation of the innate and inflammatory responses, characterized by increasing levels and impaired synthesis of pro-inflammatory cytokines. The second is associated with an impaired T helper (Th)1/Th2 balance, and most likely a shift towards Th2 responses, marked by increases in IL-10 secretion and expression.
Dr. Heffner argues that age-related changes of sympathetic nervous systems activity and cortisol, DHEA, and adreno-medullary hormones’ output may be causally linked to changes of pro- and anti-inflammatory cytokine production, and regulation of Th1 and Th2 responses.
This may contribute to the increased susceptibility of the elderly to infectious disease and pathological conditions relating to inflammation during immunosenescence.
The author concludes that developmental changes in the interplay of stress hormones and immunity should be considered to fully understand the implications of neuroendocrine stress responses for infectious/inflammatory disease risk in the elderly.
SOURCE: Immunol Allergy Clin North Am 2011, 31:95.