Helicobacter pylori binds to CD74 on gastric epithelial cells and stimulates interleukin-8 production

Ellen J. Beswick, David A. Bland, Giovanni Suarez, Carlos A. Barrera, Xuejung Fan, Victor Reyes

Research output: Contribution to journalArticle

56 Scopus citations

Abstract

The pathogenesis associated with Helicobacter pylori infection requires consistent contact with the gastric epithelium. Although several cell surface receptors have been suggested to play a role in adhesion, the bacterium-host interactions that elicit host responses are not well defined. This study investigated the interaction of H. pylori with the class II major histocompatibility complex (MHC)-associated invariant chain (Ii; CD74), which was found to be highly expressed by gastric epithelial cells. Bacterial binding was increased when CD74 surface expression was increased by gamma interferon (IFN-γ) treatment or by fibroblast cells transfected with CD74, while binding was decreased by CD74 blocking antibodies, enzyme cleavage of CD74, and CD74-coated bacteria. H. pylori was also shown to bind directly to affinity-purified CD74 in the absence of class II MHC. Cross-linking of CD74 and the engagement of CD74 were verified to stimulate IL-8 production by unrelated cell lines expressing CD74 in the absence of class II MHC. Increased CD74 expression by cells increased IL-8 production in response to H. pylori, and agents that block CD74 decreased these responses. The binding of H. pylori to CD74 presents a novel insight into an initial interaction of H. pylori with the gastric epithelium that leads to upregulation of inflammatory responses.

Original languageEnglish (US)
Pages (from-to)2736-2743
Number of pages8
JournalInfection and Immunity
Volume73
Issue number5
DOIs
StatePublished - May 2005

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ASJC Scopus subject areas

  • Immunology

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