Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism
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 unkn...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/301716 |
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| author | Su Hyuk Ko Jong Ik Jeon Young-Jeon Kim Ho Joo Yoon Hyeyoung Kim Nayoung Kim Joo Sung Kim Jung Mogg Kim |
| author_facet | Su Hyuk Ko Jong Ik Jeon Young-Jeon Kim Ho Joo Yoon Hyeyoung Kim Nayoung Kim Joo Sung Kim Jung Mogg Kim |
| author_sort | Su Hyuk Ko |
| collection | DOAJ |
| description | 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 β2 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 β2 integrin CD11/CD18 and ICAM-1. |
| format | Article |
| id | doaj-art-b0a0446a8a624a6c8eb6731b2e6ee42f |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-b0a0446a8a624a6c8eb6731b2e6ee42f2025-08-20T03:39:15ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/301716301716Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent MechanismSu Hyuk Ko0Jong Ik Jeon1Young-Jeon Kim2Ho Joo Yoon3Hyeyoung Kim4Nayoung Kim5Joo Sung Kim6Jung Mogg Kim7Department of Microbiology and Department of Biomedical Science, Hanyang University College of Medicine and Graduate School of Biomedical Science and Engineering, Sungdong-gu, Seoul 133-791, Republic of KoreaDepartment of Microbiology and Department of Biomedical Science, Hanyang University College of Medicine and Graduate School of Biomedical Science and Engineering, Sungdong-gu, Seoul 133-791, Republic of KoreaDepartment of Biotechnology, Joongbu University, Choongnam, Republic of KoreaDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of KoreaDepartment of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul, Republic of KoreaDepartment of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of KoreaDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of KoreaDepartment of Microbiology and Department of Biomedical Science, Hanyang University College of Medicine and Graduate School of Biomedical Science and Engineering, Sungdong-gu, Seoul 133-791, Republic of KoreaEosinophil 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 β2 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 β2 integrin CD11/CD18 and ICAM-1.http://dx.doi.org/10.1155/2015/301716 |
| spellingShingle | Su Hyuk Ko Jong Ik Jeon Young-Jeon Kim Ho Joo Yoon Hyeyoung Kim Nayoung Kim Joo Sung Kim Jung Mogg Kim Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism Mediators of Inflammation |
| title | Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism |
| title_full | Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism |
| title_fullStr | Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism |
| title_full_unstemmed | Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism |
| title_short | Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism |
| title_sort | helicobacter pylori outer membrane vesicle proteins induce human eosinophil degranulation via a β2 integrin cd11 cd18 and icam 1 dependent mechanism |
| url | http://dx.doi.org/10.1155/2015/301716 |
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