Annexin 1 Is Secreted in Situ During Ulcerative Colitis in Humans

N Vergnolle, P Pagès, R Guimbaud… - Inflammatory Bowel …, 2004 - academic.oup.com
N Vergnolle, P Pagès, R Guimbaud, S Chaussade, L Buéno, J Escourrou, C Coméra
Inflammatory Bowel Diseases, 2004academic.oup.com
Although annexin l exerts extracellular anti-inflammatory properties, little is known about its
release in inflammatory diseases. Here, we characterized annexin 1 secretion in ulcerative
colitis (UC) patients. Annexin 1 was detected by immunoblotting, in tissue homogenates and
supernatants of colonic biopsies incubated in culture media, and in luminal colonic
perfusates of UC patients. Annexin 1 was released by inflamed colonic biopsies from
patients having severe UC but not by biopsies from healthy colon of the same patient or by …
Abstract
Although annexin l exerts extracellular anti-inflammatory properties, little is known about its release in inflammatory diseases. Here, we characterized annexin 1 secretion in ulcerative colitis (UC) patients. Annexin 1 was detected by immunoblotting, in tissue homogenates and supernatants of colonic biopsies incubated in culture media, and in luminal colonic perfusates of UC patients. Annexin 1 was released by inflamed colonic biopsies from patients having severe UC but not by biopsies from healthy colon of the same patient or by biopsies from non-UC patients or from patients with slight or moderate UC. Annexin 1 was detected in luminal colonic perfusates of patients having moderate or slight UC but not in perfusates from control patients. The level of annexin 1 expression and secretion was unrelated to long-term glucocorticoid treatment, but annexin 1 secretion in perfusates was induced, in some patients, by short-term glucocorticoid exposure. These results show that annexin 1 is secreted endogenously in the colon of patients with UC. This secretion, which occurs both in vitro and in vivo, depends on the severity of inflammation. Given the anti-inflammatory effects of annexin 1, this protein may serve to down-regulate the inflammatory response in the course of inflammatory bowel disease.
Oxford University Press