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Attenuation of acid induced oesophagitis in VR-1 deficient mice
  1. K Fujino,
  2. S G de la Fuente,
  3. Y Takami,
  4. T Takahashi,
  5. C R Mantyh
  1. Department of Surgery, Duke University Medical Center, Durham, NC, USA
  1. Correspondence to:
    Professor C R Mantyh
    Duke University Medical Center, Box 3117, Durham, NC 27710, USA; manty001{at}


Background and aims: Activation of the vanilloid receptor subtype 1 (VR-1) results in release of proinflammatory peptides which initiate an inflammatory cascade known as neurogenic inflammation. We investigated its role in an acute model of surgically induced oesophagitis.

Methods: Oesophagitis was induced by pyloric ligation in wild-type and VR-1 deficient mice. A subset of animals were administered the VR-1 antagonist capsazepine, famotidine, or omeprazole one hour before surgery. Five hours after surgery, myeloperoxidase activity (MPO), histological damage scores, intragastric pH, and immunocytochemical analysis of substance P (SP) receptor endocytosis were determined.

Results: Oesophagitis induced knockout mice exhibited significantly lower levels of MPO activity, histological damage scores, and SP receptor endocytosis than wild-type mice. Inflammatory parameters were significantly reduced by acid inhibition and capsazepine in wild-type mice.

Conclusions: We conclude that acute acid induced oesophagitis is reduced in animals lacking VR-1. This suggests that acid induced oesophagitis may act through VR-1 and that inhibition of the receptor may reduce inflammation.

  • VR-1, vanilloid receptor subtype 1
  • GORD, gastro-oesophageal reflux disease
  • MPO, myeloperoxidase
  • NK-1, neurokinin 1
  • SP, substance P
  • PCR, polymerase chain reaction
  • HTAB, hexadecyltrimethyllammonium bromide
  • receptor
  • substance P
  • neurogenic inflammation
  • oesophagitis
  • vanilloid receptor subtype-1
  • capsaicin

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  • Conflict of interest: None declared.

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