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Eosinophil cationic protein (ECP), a cytotoxic protein contained in eosinophils granules, can contribute to various inflammatory responses. Although  Helicobacter pylori  infection increases infiltration of eosinophils, the mechanisms of eosinophil degranulation by  H. pylori  infection are largely unknown. The goal of this study was to investigate the role of  H. pylori  outer membrane vesicles (OMVs) in modulating eosinophil degranulation. We found that eosinophils treated with  H. pylori  OMVs released significantly more ECP compared with untreated controls. In addition, eosinophils cocultured with OMV-preexposed primary gastric epithelial cells exhibited significantly increased ECP release. Similarly, eosinophils cocultured with culture supernatant (CM) from primary gastric epithelial cells exposed to OMVs (OMV-CM) released significantly higher amounts of ECP compared with eosinophils cocultured with CM from unexposed control cells. Furthermore, OMVs and OMV-CM both induced the upregulation of ICAM-1 on gastric epithelial cells and  β 2 integrin CD11b on eosinophils. In addition, both transduction of  ICAM-1  shRNA into gastric epithelial cells and treatment with neutralizing mAbs to CD18 significantly decreased OMV-mediated or OMV-CM-mediated release of ECP. These results suggest that the eosinophil degranulation response to  H. pylori  OMVs occurs via a mechanism that is dependent on both  β 2 integrin CD11/CD18 and ICAM-1.

mediators of inflammation

<i>Helicobacter pylori</i>Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a<i>β</i>2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism

Helicobacter pyloriOuter Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via aβ2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism