help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Berstad, A. E.
Right arrow Articles by Brandtzaeg, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Berstad, A. E.
Right arrow Articles by Brandtzaeg, P.
(American Journal of Pathology. 1999;155:1097-1104.)
© 1999 American Society for Investigative Pathology

Regular Articles

Increased Mucosal Production of Monomeric IgA1 but No IgA1 Protease Activity in Helicobacter pylori Gastritis

Audun E. Berstad*, Mogens Kilian{dagger}, Kølbjørn N. Valnes* and Per Brandtzaeg*

From the Laboratory for Immunohistochemistry and Immunopathology,*
Institute of Pathology, University of Oslo, The National Hospital, Rikshospitalet, Oslo, Norway; and the Department of Medical Microbiology and Immunology,{dagger}
University of Aarhus, Aarhus, Denmark

Immunoglobulin A and IgM are subjected to epithelial transport only when they are produced as polymers with incorporated J chain. Immunocytes containing various Ig isotypes and associated J chain in gastric mucosa, as well as IgA-degrading protease activity in Helicobacter pylori cultures, were examined. Gastric body specimens from 15 H. pylori-positive and 14 H. pylori-negative patients were studied by paired immunofluorescence for IgA, IgA1, IgA2, IgG, or IgM and concurrent cellular J chain. H. pylori isolates were incubated with IgA1 or secretory IgA and examined by immunoelectrophoresis for cleavage products. A substantial increase of Ig-producing cells occurred in chronic gastritis, particularly in the IgA1 isotype, but H. pylori was shown to possess neither IgA1-specific nor nonspecific IgA-degrading protease activity. Regardless of infection status, reduced J chain expression was observed for all immunocyte isotypes (except for IgM) in inflamed compared with normal gastric body mucosa, the median positivity for IgA1 cells being reduced to 58.7% versus 87.9% (P = 0.0002), and for IgA2 cells to 48.9% versus 87.8% (P = 0.0002). This down-regulation of the J chain suggested that a large fraction of IgA monomers is produced in gastritis.




This article has been cited by other articles:


Home page
 Clin. Microbiol. Rev.Home page
H. M. S. Algood and T. L. Cover
Helicobacter pylori Persistence: an Overview of Interactions between H. pylori and Host Immune Defenses
Clin. Microbiol. Rev., October 1, 2006; 19(4): 597 - 613.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. A. Akhiani, K. Schon, L. E. Franzen, J. Pappo, and N. Lycke
Helicobacter pylori-Specific Antibodies Impair the Development of Gastritis, Facilitate Bacterial Colonization, and Counteract Resistance against Infection
J. Immunol., April 15, 2004; 172(8): 5024 - 5033.
[Abstract] [Full Text] [PDF]

Home page
 Microbiol. Mol. Biol. Rev.Home page
J. D. Dubreuil, G. D. Giudice, and R. Rappuoli
Helicobacter pylori Interactions with Host Serum and Extracellular Matrix Proteins: Potential Role in the Infectious Process
Microbiol. Mol. Biol. Rev., December 1, 2002; 66(4): 617 - 629.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by the American Society for Investigative Pathology.