Inflammation and stress

Townsend Letter for Doctors and Patients,  May, 2005  by Robert A. Anderson

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In response to psychological or certain physiological stressors, an inflammatory process may occur through release of neuropeptides (especially substance P or other inflammatory mediators) from sensory nerves and the activation of mast cells or other inflammatory cells. Central neuropeptides, including corticotropin releasing factor and perhaps substance P as well, initiate a systemic stress mobilization response by activating the sympathetic nervous system, hypothalamic pituitary axis, and the renin angiotensin system, thus releasing stress hormones (catecholamines, corticosteroids, growth hormone, glucagon, and renin) which, together with cytokines induced by stress, initiate the acute phase response and the induction of acute phase proteins, essential mediators of inflammation. CNS norepinephrine may also induce the acute phase response by macrophage activation and cytokine release. Increase in lipids with stress may also be a factor in macrophage activation and lipopolysaccharide release which may induce cytokines from hepatic Kupffer cells, subsequent to an enhanced absorption from the gastrointestinal tract during psychological stress. The brain is capable of initiating or inhibiting the inflammatory process. The inflammatory response is contained within the psychological stress response which was a later development in human evolution. Moreover, the same neuropeptides (i.e., CRF and possibly substance P) mediate both stress and inflammation. Cytokines evoked by either a stress or inflammatory response may utilize similar somatosensory pathways to signal the brain. Repeated episodes of acute or chronic psychogenic stress may produce chronic inflammatory changes which may result in atherosclerosis in the arteries or chronic inflammatory changes in other organs as well.

Black PH. Stress and the inflammatory response: A review of neurogenic inflammation. Brain Behav Immun 2002 Dec; 16(6):622-53

COMMENT: As delineated in this summary, derangement of immune responses related to poor management of stressors participates in altering the inflammatory responses which play major roles in atherosclerotic disease. Many theorists now think that the final event in rupture of arterial plaques is related to an acute inflammatory response. This may explain the relation of acute myocardial infarction to acute outbursts of anger. It is probably true that inflammatory attitudes are more than metaphorically related to chemical inflammatory responses in the body.

COPYRIGHT 2005 The Townsend Letter Group
COPYRIGHT 2005 Gale Group