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Inhibition of epithelial growth factor receptor signalling does not preserve epithelial barrier function after in vitro gliadin insult.

Abstract：

OBJECTIVE:In coeliac disease, small-bowel mucosal permeability is increased in response to gluten consumption. However, the signalling routes leading to such a barrier defect remain obscure. As the epidermal growth factor receptor (EGFR) pathway is up-regulated in untreated coeliac disease, and since this cascade has been related to epithelial hyperpermeability, the aim of this study was to establish whether blocking the EGFR route would restore the barrier after gliadin insult in vitro. MATERIAL AND METHODS:Epithelial barrier function was assessed by measuring transepithelial electrical resistance (TER) in Caco-2 epithelial monolayers treated with pepsin trypsin (PT)-digested gliadin with or without monoclonal antibodies against EGFR family members or by inhibitors of the EGFR pathway signalling molecules. Furthermore, tight-junctional integrity was determined by Western blotting and immunofluorescence staining of the tight-junctional protein occludin. RESULTS:PT-gliadin significantly reduced TER and the expression of occludin protein. Blocking of the EGFR signalling pathway could not prevent gliadin-triggered damage. In fact, a function-blocking monoclonal antibody against EGFR (ErbB1) actually potentiated the harmful effects of gliadin on TER. CONCLUSIONS:The epithelial barrier-disrupting properties of gliadin are independent of the EGFR signalling cascade. However, our results suggest that activation of the EGFR pathway might actually be protective against gliadin-triggered hyperpermeability. Further studies are needed to elucidate the specific gliadin-triggered signalling cascades which lead to increased epithelial permeability in coeliac disease.

journal_name

Scand J Gastroenterol

journal_title

Scandinavian journal of gastroenterology

authors

Juuti-Uusitalo K,Lindfors K,Mäki M,Patrikainen M,Isola J,Kaukinen K

doi

10.1080/00365520902898119

subject

Has Abstract

pub_date

2009-01-01 00:00:00

pages

820-5

issue

7

eissn

0036-5521

issn

1502-7708

pii

910443137

journal_volume

44

pub_type

杂志文章

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