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.
To study the distribution of TRPV1-expressing nerve fibres in oesophageal mucosal biopsies from patients with symptomatic oesophagitis and in control subjects.
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.
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.
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.
aHope Hospital, Department of Gastrointestinal Sciences, Manchester, bPeripheral Neuropathy Unit, Imperial College School of Medicine, Hammersmith Hospital, London, and cNeurology CEDD, GlaxoSmithKline, Harlow, UK.
Correspondence to Professor P. Anand, Professor of Clinical Neurology, Peripheral Neuropathy Unit, Area A, Ground Floor, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK. Tel: +44 (0)20 8383 3309/19; fax: +44 (0)20 8383 3363/8824; e-mail: email@example.com
Received 22 July 2003 Accepted 9 March 2004