Helicobacter pyloriBinds to CD74 on Gastric Epithelial Cells and Stimulates Interleukin-8 Production

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Abstract
The pathogenesis associated withHelicobacter pyloriinfection 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 ofH. pyloriwith 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. pyloriwas 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 toH. pylori, and agents that block CD74 decreased these responses. The binding ofH. pylorito CD74 presents a novel insight into an initial interaction ofH. pyloriwith the gastric epithelium that leads to upregulation of inflammatory responses.

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