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


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
Issue number5
StatePublished - May 2005


ASJC Scopus subject areas

  • Immunology

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