Immune reaction against the cytoskeleton in coeliac disease.
نویسندگان
چکیده
BACKGROUND The cytoskeleton actin network of intestinal microvilli has been found to be rapidly impaired after gluten challenge in coeliac disease (CD). The aim of this study was to investigate the presence of an immune reaction towards cytoskeleton structures such as actin filaments in CD. METHODS Eighty three antiendomysial antibody positive CD patients (52 children and 31 adults) were studied at our outpatient clinics from 1996 to 1998 using indirect immunofluorescence, ELISA, and western blotting for antiactin (AAA) and antitissue transglutaminase (TGA) antibodies before and after a gluten free diet (GFD). Sixteen patients with smooth muscle antibody positive autoimmune hepatitis, 21 with inflammatory bowel diseases, seven with small bowel bacterial overgrowth, and 60 healthy subjects were studied as controls. RESULTS Fifty nine of 83 CD patients (28/31 adults (90.3%); 31/52 children (59.6%)) were positive for IgA and/or IgG AAA. Seventy seven (92.7%) were positive for IgA TGA. IgA AAA were strongly correlated with more severe degrees of intestinal villous atrophy (p<0.0001; relative risk 86.17). After a GFD, AAA became undetectable within five months. CONCLUSIONS Apart from the immune reaction against the extracellular matrix, we have described an immune reaction against the cytoskeleton in both children and adults with CD. As AAA are strongly associated with more severe degrees of villous atrophy, they may represent a useful serological marker of severe intestinal atrophy in CD.
منابع مشابه
BINDAZYMETM Human Anti-Gliadin EIA Kit For in-vitro diagnostic use Product code: IgG: MK135 IgA: MK136 IgG or IgA: MK137
Coeliac disease is an inflammatory disease of the small intestine caused by ingestion of wheat gluten or related proteins from rye or barley. In the small intestine, ingested gluten is broken down into gliadin peptides which are deamidated by the enzyme tissue transglutaminase (tTg) resulting in the substitution of glutamine amino acid residues with glutamic acid. These modified gliadin peptide...
متن کاملBreast milk against coeliac disease.
Coeliac disease is a multifactorial disorder developing as a result of a complex interplay between genetic and environmental factors. HLA and non-HLA genes are involved, and gluten is obviously a critical environmental factor as the disease goes into remission when gluten is eliminated from the diet. The important case control study by Ivarsson et al concludes that feeding with breast milk when...
متن کاملCoeliac Disease With Rheumatoid Arthritis: An Unusual Association
Coeliac disease has a significant association with many autoimmune disorders. It shares many common genetic and immunological features with other autoimmune diseases. Gluten, a gut-derived antigen, is the driver of the autoimmunity seen in coeliac disease. The altered intestinal permeability found in coeliac patients, coupled with a genetic predisposition and altered immunological response, may...
متن کاملA young girl with H syndrome and coeliac disease
H syndrome is an autosomal recessive genodermatosis with reports dating back to the last decade. This syndrome is caused by mutations in the SCL29A3 gene. The clinical characteristics of this syndrome consist of dermatological manifestations, including hyperpigmented, hypertrichotic, and indurated patches and plaques. It affects various systems by causing heart anomalies, hepatosplenomegaly, hy...
متن کاملType 1 Diabetes Mellitus, Celiac Disease, and Selective IgA Deficiency: a Case Report
Patients with Type 1 diabetes mellitus have a high prevalence of coeliac disease, symptoms of which are often mild, atypical, or absent. Untreated coeliac disease is associated with an increased risk of malignancy, particularly of lymphoma. Therefore, we report a 9-year-old girl with Coeliac disease, diabetes type 1 and Selective IgA deficiency. A 9-year-old female patient presented in august 2...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Gut
دوره 47 4 شماره
صفحات -
تاریخ انتشار 2000