Neuroimmune mechanisms of intestinal responses to stress. Role of corticotropin-releasing factor and neurotensin.
Previous studies showed that exposure of experimental animals to immobilization stress increases colonic motility and that these effects are mediated by release of corticotropin-releasing factor ( CRF), Studies from our laboratory showed that 30-min immobilization stress of rats caused several not previously described colonic responses to stress, including increased colonic mucin and prostaglandin E2 (PGE2) secretion, increased colonic mucosal levels of cyclooxygenase-2 ( COX-2) mRNA, and degranulation of colonic mast cells. These stress-associated colonic changes were reproduced by intravenous or intracerebral injection of CRF in conscious, nonstressed rats. Furthermore, pretreatment of rats with the CRF antagonist alpha-helical CRF9-41, hexamethonium, or the mast cell stabilizer lodoxamide inhibited our observed colon responses to immobilization stress. Our results indicate that CRF released during immobilization stress increases colonic transit via a neuronal pathway and stimulates colonic mucin release via activation of neurons and colonic mast cells. These results provide support for an important role for CRF in stress-mediated colonic responses and a link between the nervous and the immune systems.[1]References
- Neuroimmune mechanisms of intestinal responses to stress. Role of corticotropin-releasing factor and neurotensin. Pothoulakis, C., Castagliuolo, I., Leeman, S.E. Ann. N. Y. Acad. Sci. (1998) [Pubmed]
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