Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/18673
Title: Anti-inflammatory effects of pancreatitis associated protein in inflammatory bowel disease
Author: Gironella Cos, Meritxell
Iovanna, J. L.
Sans i Cuffí, Miquel
Gil, F.
Peñalva, M.
Closa i Autet, Daniel, 1961-
Miquel Morera, Rosa
Piqué, J. M. (Piqué Badía)
Panés Díaz, Julià
Keywords: Malalties inflamatòries intestinals
Pancreatitis
Proteïnes
Inflammatory bowel diseases
Pancreatitis
Proteins
Issue Date: 2005
Publisher: BMJ Group
Abstract: Background and aims: Increased pancreatitis associated protein (PAP) mRNA has been reported in active inflammatory bowel disease (IBD). The aims of the current study were to characterise PAP production in IBD and the effects of PAP on inflammation. Patients and methods: Serum PAP levels were determined in healthy controls (n¿=¿29), inflammatory controls (n¿=¿14), and IBD patients (n¿=¿171). Ex vivo PAP secretion in intestinal tissue was measured in 56 IBD patients and 13 healthy controls. Cellular origin of PAP was determined by immunohistochemistry. The effects of exogenous PAP on nuclear factor ¿B (NF¿B) activation, proinflammatory cytokine production, and endothelial adhesion molecule expression were also analysed ex vivo. Results: Patients with active IBD had increased serum PAP levels compared with controls, and these levels correlated with clinical and endoscopic disease severity. Ex vivo intestinal PAP synthesis was increased in active IBD and correlated with endoscopic and histological severity of inflammatory lesions. PAP localised to colonic Paneth cells. Incubation of mucosa from active Crohn¿s disease with PAP dose dependently reduced proinflammatory cytokines secretion. PAP prevented TNF-¿ induced NF¿B activation in monocytic, epithelial, and endothelial cells and reduced proinflammatory cytokine mRNA levels and adhesion molecule expression. Conclusions: PAP is synthesised by Paneth cells and is overexpressed in colonic tissue of active IBD. PAP inhibits NF¿B activation and downregulates cytokine production and adhesion molecule expression in inflamed tissue. It may represent an anti-inflammatory mechanism and new therapeutic strategy in IBD.
Note: Reproducció digital del document publicat a: http://dx.doi.org/10.1136/gut.2004.056309
It is part of: Gut, 2005, vol. 54, núm. 9, p. 1244-1253
URI: http://hdl.handle.net/2445/18673
ISSN: 0017-5749
Appears in Collections:Articles publicats en revistes (Medicina)

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