Danish Medical Bulletin - No. 4. November 2004. Vol. 51 Page 441.

ABSTRACT OF PhD DISSERTATION

Regulations of inducible
nitric oxide synthase
in collagenous colitis

Lars Andresen, Msc

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This PhD dissertation was accepted by the Faculty of Health Sciences of the University of Copenhagen, and defended on October 5, 2004.

Official opponents: Niels-Erik Møllegaard, Ove Andersen and Brendan Whittle, UK.

Tutor: Jørgen Rask-Madsen.

Correspondence: Lars Andresen, Dept. of Gastroenterology, Herlev University Hospital, Herlev Ringvej 75, 2730 Herlev, Denmark.
E-mail: laand@herlevhosp.kbhamt.dk

Dan Med Bull 2004;51:441.

ABSTRACT

This work was carried out at the Department of Gastroenterology, Herlev University Hospital, and the Clinical Research Unit, H:S Hvidovre Hospital, Denmark.

Production of nitric oxide and expression of inducible nitric oxide synthase (iNOS) are greatly increased in the inflamed colonic mucosa.

Collagenous colitis is an inflammatory bowel disease of unknown aetiology characterized clinically by chronic watery diarrhoea in the absence of mucosal injury and histologically by infiltration of lymphocytes and plasma cells in the lamina propria, a thickened subepithelial layer of collagen, and excess of intraepithelial lymphocytes. This condition is associated with similarly high production rates of nitric oxide as observed in ulcerative colitis, which is characterized by relapsing, injurious inflammation of the colorectal mucosa.

In the present comparative study, the expression of iNOS and the activity of its inducer, nuclear factor kappa B (NF- κ B) in colonic mucosal biopsies from patients with collagenous colitis, ulcerative colitis (positive controls) or functional bowel disease (negative controls) have been investigated.

The results demonstrate high expression of iNOS and activation of NF- κ B both in collagenous and ulcerative colitis. As injurious inflammation never occurs in patients with collagenous colitis, it seems unlikely that activation of the above proteins per se mediates mucosal damage in colonic inflammation.


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