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