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dc.contributor.author고수혁-
dc.date.accessioned2018-05-21T06:24:11Z-
dc.date.available2018-05-21T06:24:11Z-
dc.date.issued2016-05-
dc.identifier.citationINFECTION AND IMMUNITY, v. 84, NO 8, Page. 2162-2174en_US
dc.identifier.issn0019-9567-
dc.identifier.issn1098-5522-
dc.identifier.urihttp://iai.asm.org/content/84/8/2162-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/71421-
dc.description.abstractHelicobacter pylori sheds outer membrane vesicles (OMVs) that contain many surface elements of bacteria. Dendritic cells (DCs) play a major role in directing the nature of adaptive immune responses against H. pylori, and heme oxygenase-1 (HO-1) has been implicated in regulating function of DCs. In addition, HO-1 is important for adaptive immunity and the stress response. Although H. pylori-derived OMVs may contribute to the pathogenesis of H. pylori infection, responses of DCs to OMVs have not been elucidated. In the present study, we investigated the role of H. pylori-derived crude OMVs in modulating the expression of HO-1 in DCs. Exposure of DCs to crude H. pylori OMVs upregulated HO-1 expression. Crude OMVs obtained from a cagA-negative isogenic mutant strain induced less HO-1 expression than OMVs obtained from a wild-type strain. Crude H. pylori OMVs activated signals of transcription factors such as NF-kappa B, AP-1, and Nrf2. Suppression of NF-kappa B or Nrf2 resulted in significant attenuation of crude OMV-induced HO-1 expression. Crude OMVs increased the phosphorylation of Akt and downstream target molecules of mammalian target of rapamycin (mTOR), such as S6 kinase 1 (S6K1). Suppression of Akt resulted in inhibition of crude OMV-induced Nrf2-dependent HO-1 expression. Furthermore, suppression of mTOR was associated with inhibition of I kappa B kinase (IKK), NF-kappa B, and HO-1 expression in crude OMV-exposed DCs. These results suggest that H. pylori-derived OMVs regulate HO-1 expression through two different pathways in DCs, Akt-Nrf2 and mTOR-IKK-NF-kappa B signaling. Following this induction, increased HO-1 expression in DCs may modulate inflammatory responses in H. pylori infection.en_US
dc.description.sponsorshipThe Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (MEST) (NRF-2015R1D1A1A01058565) supported this research, along with a grant from the Medical Research Center (MRC program no. 2008-0062287), funded by NRF of the Ministry of Science, ICT, and Future Planning, Republic of Korea.en_US
dc.language.isoenen_US
dc.publisherAMER SOC MICROBIOLOGYen_US
dc.subjectGASTRIC EPITHELIAL-CELLSen_US
dc.subjectCLOSTRIDIUM-DIFFICILE TOXINen_US
dc.subjectVACUOLATING CYTOTOXINen_US
dc.subjectFUNCTIONAL-CHARACTERIZATIONen_US
dc.subjectIMMUNE-RESPONSEen_US
dc.subjectHOST RESPONSEen_US
dc.subjectMATURATIONen_US
dc.subjectPROTEINen_US
dc.subjectEXPRESSIONen_US
dc.subjectINFECTIONen_US
dc.titleCrude Preparations of Helicobacter pylori Outer Membrane Vesicles Induce Upregulation of Heme Oxygenase-1 via Activating Akt-Nrf2 and mTOR-I kappa B Kinase-NF-kappa B Pathways in Dendritic Cellsen_US
dc.typeArticleen_US
dc.relation.no8-
dc.relation.volume84-
dc.identifier.doi10.1128/IAI.00190-16-
dc.relation.page2162-2174-
dc.relation.journalINFECTION AND IMMUNITY-
dc.contributor.googleauthorKo, Su Hyuk-
dc.contributor.googleauthorRho, Da Jeong-
dc.contributor.googleauthorJeon, Jong Ik-
dc.contributor.googleauthorKim, Young-Jeon-
dc.contributor.googleauthorWoo, Hyun Ae-
dc.contributor.googleauthorKim, Nayoung-
dc.contributor.googleauthorKim, Jung Mogg-
dc.relation.code2016001121-
dc.sector.campusS-
dc.sector.daehakRESEARCH INSTITUTE[S]-
dc.sector.departmentHBRI-
dc.identifier.pidztizen-
dc.identifier.researcherIDA-8207-2017-


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