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(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.




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