Author
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Eicher, Susan |
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BURTON, J - MICHIGAN STATE UNIVERSITY |
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Submitted to: Encyclopedia of Animal Science
Publication Type: Book / Chapter Publication Acceptance Date: 10/21/2003 Publication Date: 3/31/2010 Citation: Eicher, S. 2010. the Encyclopedia of Applied Animal Behaviour and Welfare, CABI No. Am. Office, Cambridge, MA. Available: www.cabi.org Interpretive Summary: Stress has been difficult to define because of its dual function in life. It can be a positive influence that satisfies a need for excitement (environmental enrichment) or a negative influence that interferes with homeostasis and life functions. Moberg referred to the latter as a state of distress. Our use of stress here will refer to this darker side of stress. The interaction between stress and the immune system is a conundrum because of the negative impact that stress can have on immune functions and because active immune responses can be stressors in and of themselves. Stress can also activate or suppress immune responses depending on the degree and persistence of the stressor; the species, age, sex, and genetics of the subject; and the immune cells that are the targets of the stress. Not all stressors result in the same immune response to stress, such as isolation compared to restraint stress. But, in general, most psychological and environmental stressors lead to impaired immune functions, especially those that regulate inflammatory and cytotoxic responses. The deleterious effects of stress are readily observed at an early gene expression level in cells of the innate (not requiring prior exposure to foreign antigen) and adaptive (requiring prior exposure to foreign antigen) immune systems. Thus, stress-immune interactions usually have significant physiological consequences even before gross behavioral or pathogenic changes are observed. This information will provide animal science students and researchers with current information on the impact of stress on immunity. Technical Abstract: Glucocorticoids are the main effector endpoint of the neuroendocrine response to stressors and result from activation of the hypothalamus-pituitary-adrenal axis. Another pathway that mediates stress responses in animals is the sympatho-adrenal axis. Glucocorticoids (GC) act by regulating expression of multiple GC-sensitive genes and thus the expression of proteins that determine the phenotype and function of cells responsible for coordinating the body's response to stress. Gene expression regulation results from the binding of GC to its receptor (GR) found primarily in the cytoplasm of target cells, with subsequent translocation of the hormone-activated GR into the nucleus, where it has its major effect. Thus, blood cortisol concentrations resulting from a stress response can have pronounced effects on immunity through altered expression of hundreds of immune cell genes. More immediate immune regulation is induced by stress through the actions of catecholamines (sympatho-adrenal axis). Compared to glucocorticoids, however, relatively little information is available on the molecular mechanisms used by catecholamines to change leukocyte biology and immune responses. Changes in leukocyte numbers and their altered ability to communicate with each other through chemokines, cytokines, adhesion molecules, MHC complexes, and other inflammatory mediators occur in most farm animals when blood glucocorticoids and catacholamine concentrations increase, leaving stressed animals at risk for diseases caused by bacteria, virus, and parasites. Thus, the reduction of management practices that induce pronounced or chronic stress is critical to enhance animal well-being. |
