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Small intestine
Keratinocyte growth factor and coeliac disease
  1. V M Salvatia,
  2. M Bajaj-Elliottb,
  3. R Poulsomc,
  4. G Mazzarellad,
  5. K E A Lundine,
  6. E M Nilsenf,
  7. R Tronconea,
  8. T T MacDonaldg
  1. aDepartment of Paediatrics and European Laboratory for the Investigation of Food-Induced Diseases, University Federico II, Naples, Italy, bDepartment of Adult and Paediatric Gastroenterology, St Bartholomew's and the Royal London School of Medicine and Dentistry, London, UK, cHistopathology Unit, Imperial Cancer Research Fund, London, UK, dInstitute of Food, Science, and Technology, CNR Avellino, Italy, eInstitute of Immunology, The National Hospital, University of Oslo, Norway, fLIIPAT Institute of Pathology, The National Hospital, University of Oslo, Norway, gDivision of Infection, Inflammation, and Repair, University of Southampton, School of Medicine, Southampton, UK
  1. T T MacDonald, Division of Infection, Inflammation, and Repair, School of Medicine, Southampton General Hospital, MailPoint 813, Level E, South Academic Block, Tremona Road, Southampton SO16 6YD, UK.t.t.macdonald{at}soton.ac.uk

Abstract

BACKGROUND Coeliac disease is characterised by increased epithelial renewal associated with a mucosal T cell response to gliadin. Keratinocyte growth factor (KGF) is produced by cytokine activated gut stromal cells and may be a link between mucosal T cell activation in untreated coeliac disease and epithelial hyperplasia.

AIMS To characterise expression of KGF in coeliac disease.

METHODS KGF transcripts in coeliac disease were measured by quantitative competitive reverse transcription-polymerase chain reaction (RT-PCR) and localised using in situ hybridisation. KGF production by gluten reactive CD4+ T cell clones was examined. In addition, KGF transcripts were measured following ex vivo challenge of coeliac biopsies with a peptic-tryptic digest of gliadin.

RESULTS KGF transcripts were elevated in coeliac biopsies compared with normal controls but were not different from non-coeliac disease controls. By in situ hybridisation, KGF mRNA containing cells were present in the upper half of the lamina propria, most abundantly just under the epithelium. There was no signal from cells within the epithelium. Gluten reactive T cell clones did not make KGF. In vitro challenge of coeliac biopsies generated a strong interferon γ response but a specific KGF response could not be detected because of an extremely high number of KGF transcripts in all cultured biopsies.

CONCLUSIONS KGF is overexpressed in coeliac biopsies and in tissues with non-coeliac enteropathy. No evidence was found for KGF production by intraepithelial lymphocytes or lamina propria T cells.

  • coeliac disease
  • keratinocyte growth factor
  • mRNA expression

  • Abbreviations used in this paper

    CD
    coeliac disease
    KGF (FGF-7)
    keratinocyte growth factor
    IEL
    intraepithelial lymphocytes
    NCE
    non-coeliac enteropathy
    RT-PCR
    reverse transcription-polymerase chain reaction
    IFN-γ
    interferon γ
    IBD
    inflammatory bowel disease
    LPL
    lamina propria T cells

    • https://doi.org/10.1136/gut.49.2.176

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    • Abbreviations used in this paper

      CD
      coeliac disease
      KGF (FGF-7)
      keratinocyte growth factor
      IEL
      intraepithelial lymphocytes
      NCE
      non-coeliac enteropathy
      RT-PCR
      reverse transcription-polymerase chain reaction
      IFN-γ
      interferon γ
      IBD
      inflammatory bowel disease
      LPL
      lamina propria T cells
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