Lack of interaction between psychological stress and DSS-induced colitis affecting colonic sensitivity during colorectal distension in mice.
Inflammation and stress have been associated to colorectal hypersensitivity in functional gastrointestinal disorders. We explored if colonic inflammation and stress, alone or combined, participate in the development of visceral hypersensitivity in a mouse model. First, female mice were exposed to 3% dextran sulphate sodium (DSS, 5 days) to induce chronic colitis, followed by repeated psychological stress (water avoidance stress, WAS; 1 h daily/10 days). In a separate experiment, female mice were subjected to WAS and thereafter received 3% DSS. Colitis was evaluated at necropsy. Faecal pellet output served as a marker of stress effect on colonic motility. Visceral pain was assessed at fixed time-points monitoring abdominal contractions during colorectal distension (CRD). DSS provoked a mild chronic colitis that was not affected by previous WAS or aggravated by subsequent stress. WAS induced a significant increase in pellet output, although the response was attenuated in animals with colitis. Responses to CRD were similar in all experimental groups, with transient hyperalgesia observed only during acute colitis. Under the present conditions, neither colitis nor stress, alone or in combination, significantly affected the responses to CRD in mice, suggesting that there is not a direct relationship between inflammation and stress and the development of visceral hypersensitivity.
Larsson
M H
MH
AstraZeneca R&D, Mölndal, Sweden.
Miketa
A
A
Martinez
V
V
D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000503:physiopathology*; D003106:Colon / Q000503:physiopathology*; D016264:Dextran Sulfate; D004108:Dilatation, Pathologic / Q000503:physiopathology; D005260:Female; D005769:Gastrointestinal Motility; D051379:Mice; D008810:Mice, Inbred C57BL; D017288:Pain Threshold; D013315:Stress, Psychological / Q000503:physiopathology*
D016264:Dextran Sulfate