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Is Candida albicans a trigger in the onset of coeliac disease?

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Author: Nieuwenhuizen, W.F. · Pieters, R.H.H. · Knippels, L.M.J. · Jansen, M.C.J.F. · Koppelman, S.J.
Type:article
Date:2003
Source:Lancet, 9375, 361, 2152-2154
Identifier: 237150
doi: doi:10.1016/S0140-6736(03)13695-1
Keywords: Biology Toxicology · Food technology · autoantibody · blood clotting factor 13a · epitope · gliadin · gluten · hyphal wall protein 1 · protein glutamine gamma glutamyltransferase · unclassified drug · virulence factor · amino acid sequence · antibody production · article · autoimmune disease · Candida albicans · candidiasis · celiac disease · covalent bond · enzyme activity · genetic predisposition · human · immunoreactivity · intestine epithelium · intestine flora · nonhuman · pathophysiology · priority journal · protein expression · sequence analysis · sequence homology · Antibody Formation · Candida albicans · Celiac Disease · Fungal Proteins · Genetic Predisposition to Disease · Gliadin · Humans · Intestinal Mucosa · Membrane Glycoproteins · Transglutaminases · Virulence

Abstract

Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans - hyphal wall protein 1 (HWP1) - contains aminoacid sequences that are identical or highly homologous to known coeliac disease-related α-gliadin and γ-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium.