Neurokinin-1 receptor expression in inflammatory bowel disease: molecular quantitation and localisation. Issue 3 (1st September 2000)

• Record Type: Journal Article
• Authors: Goode, T; O'Connell, J; Anton, P; Wong, H; Reeve, J; O'Sullivan, G C; Collins, J K; Shanahan, F
• Is Part Of: Gut. Volume 47:Issue 3(2000)
• Page Start: 387
• Page End: 396
• Publication Date: 2000-09-01
• Subjects: substance P -- neurokinin-1 receptor -- inflammatory bowel disease; Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.47.3.387
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : BACKGROUND: Substantial evidence implicates the neuropeptide substance P (SP) in mucosal immunoinflammatory responses. Autoradiographic studies have suggested a disturbance in SP receptor expression in inflammatory bowel disease (IBD). AIMS: Because of technical limitations such as poor cellular resolution with autoradiography, we used molecular methods to specifically localise the cellular expression of the neurokinin-1 receptor (NK-1R) in IBD colon, and to quantitate NK-1R mRNA expression levels therein. METHODS: In situ hybridisation and immunohistochemistry were used to localise NK-1R mRNA and protein, respectively, in normal, ulcerative colitis (UC), and Crohn's disease (CD) colonic resections. NK-1R mRNA expression levels of normal, UC, and CD mucosal biopsies were quantitated by competitive reverse transcription-polymerase chain reaction. RESULTS: NK-1R expression was localised to lamina propria mononuclear cells, epithelium, submucosal vasculature, smooth muscle, and myenteric plexus of normal and IBD colon. No ectopic NK-1R expression was observed in IBD. However, we found increased numbers of NK-1R expressing lymphoid cells in IBD tissue, aberrant negative epithelial expression of NK-1R in UC, and increased expression of NK-1R in CD myenteric plexus. Quantitation of NK-1R mRNA expression in IBD colonic mucosal biopsies revealed marked upregulation of NK-1R mRNA levels compared with non-inflamed mucosal expression levels (p<0.01). CONCLUSIONS: This report demonstrates the strategic localisation and upregulation of NK-1R expression in IBD colon, and thereby suggests the involvement of substance P in the pathophysiological symptoms of IBD.