Abstracts: ESPGHAN-NASPGN 5th Joint Meeting
ANTI-ACTIN STRESS FIBRES ANTIBODIES IN COELIAC DISEASE
Background Coeliac disease (CD) is a gluten-sensitive enteropathy characterised by several features of autoimmunity. In CD patients gluten causes the disorganisation and disappearance of actin filaments (AF), the main protein structures of the enterocyte cytoskeleton1. The aim of this study was to investigate if this intestinal mucosa damage is associated to the presence of a humoral immunoreaction against AF. Methods 55 CD patients(ESPGHAN criteria; mean age: 7.6 years) positive for antigliadin (AGA), anti-reticulin (ARA), anti-jejunal (JAB), anti-endomysial (AEA) and anti-transglutaminase (TGA) antibodies were studied by indirect immunofluorescence (IF), ELISA and Western-blotting (WB) for anti-AF antibodies (AFA) before and after a gluten-free diet. Ten patients with Crohn's disease and 60 healthy children were studied as controls.Results In IF on HEp-2 cells, 33 (59%) CD patients were positive for AFA. No positivity was obtained in ELISA or WB with the globular actin. An immunofluorescent pattern involving the surface epithelium of the intestinal mucosa was observed on primate small bowel sections. Absorption studies with actin and TG confirmed antigen specificity. Presence of AFA was associated with severe villi atrophy (p<0.001). After the gluten-free diet AFA became undetectable within 4-5 months. Conclusions Besides autoantibodies against smooth muscle connective tissue, i.e. AEA, extracellular matrix, ARA, and basement membrane, JAB, of the lamina propria, also autoantibodies reacting to actin flaments of surface epithelium, AFA, are present in CD. Our data show that the most severe degree of tissue damage is characterised by the presence of AFA, that may represent a useful serological marker of intestinal villous atrophy in CD. This could be a very important clinical datum especially when dealing with young patients in whom invasive diagnostic procedures such as intestinal biopsies could no longer be necessary.
1. Sjolander A, Magnusson KE. Eur. J. Cell. Biol. 1988; 47:32-35
GASTROENTEROLOGY© Lippincott-Raven Publishers