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Increased capsaicin receptor TRPV1 nerve fibres in the inflamed human oesophagus

Authors :
Paul Facer
John B. Davis
Qasim Aziz
Philip J Matthews
Praveen Anand
David G. Thompson
Source :
European Journal of Gastroenterology & Hepatology. 16:897-902
Publication Year :
2004
Publisher :
Ovid Technologies (Wolters Kluwer Health), 2004.

Abstract

Background Gastro-oesophageal reflux disease (GORD) patients commonly describe symptoms of heartburn and chest pain. The capsaicin receptor vanilloid receptor 1 (TRPV1) (VR1) is a cation channel expressed by sensory neurones and activated by heat, acid pH and ethanol, which may trigger burning pain. Aim To study the distribution of TRPV1-expressing nerve fibres in oesophageal mucosal biopsies from patients with symptomatic oesophagitis and in control subjects. Methods Biopsies were taken at gastroscopy from the distal oesophagus of seven symptomatic oesophagitis patients and seven asymptomatic patients undergoing investigation for iron-deficiency anaemia. These biopsies were studied by immunohistochemistry using affinity-purified antibodies to TRPV1 and to the neuronal marker peripherin. The density of oesophageal epithelial TRPV1 innervation was assessed by calculating the proportion of papillae in each oesophageal epithelium biopsy specimen containing TRPV1-immunoreactive fibres. Results TRPV1-immunoreactive nerves were distributed within the lamina propria in healthy subjects and in oesophagitis patients. The percentage of papillae positive for TRPV1 was elevated in oesophagitis patients compared with controls. Peripherin fibre density was not significantly different between the groups. Conclusions TRPV1-immunoreactive sensory nerve fibres are expressed in human oesophageal mucosa both in health and in disease. Increased TRPV1 expression in the inflamed oesophagus may mediate the heartburn in oesophagitis, and TRPV1 blockers may provide novel treatment.

Details

ISSN :
0954691X
Volume :
16
Database :
OpenAIRE
Journal :
European Journal of Gastroenterology & Hepatology
Accession number :
edsair.doi.dedup.....ab30f2a2a8bedb6dd9d514cc0b97943a