BACKGROUND: Most antigens reach the immune system through mucosae. Gastrointestinal mucosa is a barrier for alimentary antigens. Inflammatory processes, such as Helicobacter pylori-associated gastritis, could alter the integrity of the gastric barrier, increase the mucosal permeability, and enhance crossing of food antigens which may stimulate allergic reactions. PURPOSE: The aim of this study was to establish whether patients with symptomatic food allergy and detectable immunoglobulin E (IgE) to alimentary antigens were infected by Helicobacter pylori more often than controls, and to determine the phenotype of the infecting Helicobacter pylori. PATIENTS AND METHODS: Thirty-eight consecutive patients with symptomatic food allergy and serum IgE to alimentary antigens, and 53 consecutive age-matched controls (subjects without food allergy and detectable levels of IgE anti-alimentary antigens) living in the same area and attending the same institution were investigated serologically to determine the prevalence of Helicobacter pylori infection, and an immune response to CagA, a marker of the most pathogenic strains. IgE to alimentary allergens were measured by a commercial kit. RESULTS: The prevalence of Helicobacter pylori infection in patients with food allergy and controls was similar (42.1% and 47.1%, respectively). Anti-CagA antibodies in Helicobacter pylori-infected persons were detected in 62.5% of patients with food allergy, and 28.0% of controls (p = 0.030, odds ratio = 4.29, RR = 2.23). The mean IgE level to the most common alimentary antigens was increased in CagA-positive, with respect to the CagA-negative, patients. CONCLUSIONS: The enhanced mucosal and inflammatory lesions commonly found in individuals infected by CagA-positive Helicobacter pylori strains could increase the epithelial permeability and render non-selective the passage of allergens which, in atopic persons, could directly stimulate an IgE response. Infection by CagA-positive Helicobacter pylori may increase the risk of food allergy.
BACKGROUND: Most antigens reach the immune system through mucosae. Gastrointestinal mucosa is a barrier for alimentary antigens. Inflammatory processes, such as Helicobacter pylori-associated gastritis, could alter the integrity of the gastric barrier, increase the mucosal permeability, and enhance crossing of food antigens which may stimulate allergic reactions. PURPOSE: The aim of this study was to establish whether patients with symptomatic food allergy and detectable immunoglobulin E (IgE) to alimentary antigens were infected by Helicobacter pylori more often than controls, and to determine the phenotype of the infecting Helicobacter pylori. PATIENTS AND METHODS: Thirty-eight consecutive patients with symptomatic food allergy and serum IgE to alimentary antigens, and 53 consecutive age-matched controls (subjects without food allergy and detectable levels of IgE anti-alimentary antigens) living in the same area and attending the same institution were investigated serologically to determine the prevalence of Helicobacter pylori infection, and an immune response to CagA, a marker of the most pathogenic strains. IgE to alimentary allergens were measured by a commercial kit. RESULTS: The prevalence of Helicobacter pylori infection in patients with food allergy and controls was similar (42.1% and 47.1%, respectively). Anti-CagA antibodies in Helicobacter pylori-infected persons were detected in 62.5% of patients with food allergy, and 28.0% of controls (p = 0.030, odds ratio = 4.29, RR = 2.23). The mean IgE level to the most common alimentary antigens was increased in CagA-positive, with respect to the CagA-negative, patients. CONCLUSIONS: The enhanced mucosal and inflammatory lesions commonly found in individuals infected by CagA-positive Helicobacter pylori strains could increase the epithelial permeability and render non-selective the passage of allergens which, in atopic persons, could directly stimulate an IgE response. Infection by CagA-positive Helicobacter pylori may increase the risk of food allergy.
Authors: Jason P Fedwick; Tamia K Lapointe; Jonathan B Meddings; Philip M Sherman; Andre G Buret Journal: Infect Immun Date: 2005-12 Impact factor: 3.441
Authors: Eva Untersmayr; Susanne C Diesner; Gertie Janneke Oostingh; Kathrin Selzle; Tobias Pfaller; Cornelia Schultz; Yingyi Zhang; Durga Krishnamurthy; Philipp Starkl; Regina Knittelfelder; Elisabeth Förster-Waldl; Arnold Pollak; Otto Scheiner; Ulrich Pöschl; Erika Jensen-Jarolim; Albert Duschl Journal: PLoS One Date: 2010-12-02 Impact factor: 3.240