<i>Helicobacter pylori</i>Binds to CD74 on Gastric Epithelial Cells and Stimulates Interleukin-8 Production

抄録

<jats:title>ABSTRACT</jats:title><jats:p>The pathogenesis associated with<jats:italic>Helicobacter pylori</jats:italic>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<jats:italic>H. pylori</jats:italic>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.<jats:italic>H. pylori</jats:italic>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<jats:italic>H. pylori</jats:italic>, and agents that block CD74 decreased these responses. The binding of<jats:italic>H. pylori</jats:italic>to CD74 presents a novel insight into an initial interaction of<jats:italic>H. pylori</jats:italic>with the gastric epithelium that leads to upregulation of inflammatory responses.</jats:p>

収録刊行物

被引用文献 (5)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ