Show simple item record

dc.contributor.authorAbdissa, Ketema
dc.contributor.authorNerlich, Andreas
dc.contributor.authorBeineke, Andreas
dc.contributor.authorRuangkiattikul, Nanthapon
dc.contributor.authorPawar, Vinay
dc.contributor.authorHeise, Ulrike
dc.contributor.authorJanze, Nina
dc.contributor.authorFalk, Christine
dc.contributor.authorBruder, Dunja
dc.contributor.authorSchleicher, Ulrike
dc.contributor.authorBogdan, Christian
dc.contributor.authorWeiss, Siegfried
dc.contributor.authorGoethe, Ralph
dc.date.accessioned2018-12-05T13:23:36Z
dc.date.available2018-12-05T13:23:36Z
dc.date.issued2018-01-01
dc.identifier.issn1664-3224
dc.identifier.pmid30386330
dc.identifier.doi10.3389/fimmu.2018.02317
dc.identifier.urihttp://hdl.handle.net/10033/621604
dc.description.abstractThe Gram-negative bacterium, Helicobacter pylori, causes chronic gastritis, peptic ulcers, and gastric cancer in humans. Although the gastric epithelium is the primary site of H. pylori colonization, H. pylori can gain access to deeper tissues. Concurring with this notion, H. pylori has been found in the vicinity of endothelial cells in gastric submucosa. Endothelial cells play crucial roles in innate immune response, wound healing and tumorigenesis. This study examines the molecular mechanisms by which H. pylori interacts with and triggers inflammatory responses in endothelial cells. We observed that H. pylori infection of primary human endothelial cells stimulated secretion of the key inflammatory cytokines, interleukin-6 (IL-6) and interleukin-8 (IL-8). In particular, IL-8, a potent chemokine and angiogenic factor, was secreted by H. pylori-infected endothelial cells to levels ~10- to 20-fold higher than that typically observed in H. pylori-infected gastric epithelial cells. These inflammatory responses were triggered by the H. pylori type IV secretion system (T4SS) and the T4SS-associated adhesin CagL, but not the translocation substrate CagA. Moreover, in contrast to integrin α5β1 playing an essential role in IL-8 induction by H. pylori upon infection of gastric epithelial cells, both integrin α5β1 and integrin αvβ3 were dispensable for IL-8 induction in H. pylori-infected endothelial cells. However, epidermal growth factor receptor (EGFR) is crucial for mediating the potent H. pylori-induced IL-8 response in endothelial cells. This study reveals a novel mechanism by which the H. pylori T4SS and its adhesin subunit, CagL, may contribute to H. pylori pathogenesis by stimulating the endothelial innate immune responses, while highlighting EGFR as a potential therapeutic target for controlling H. pylori-induced inflammation. Introductionen_US
dc.publisherDrontiersen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectArg1en_US
dc.subjectMDSCen_US
dc.subjectNos2en_US
dc.subjectT cellsen_US
dc.subjectdendritic cellsen_US
dc.subjectiNOSen_US
dc.subjectnon-tuberculous mycobacteriaen_US
dc.titlePresence of Infected Gr-1CD11bCD11c Monocytic Myeloid Derived Suppressor Cells Subverts T Cell Response and Is Associated With Impaired Dendritic Cell Function in -Infected Mice.en_US
dc.typeArticleen_US
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
refterms.dateFOA2018-12-05T13:23:40Z
dc.source.journaltitleFrontiers in immunology


Files in this item

Thumbnail
Name:
Ketema et al.pdf
Size:
5.924Mb
Format:
PDF
Description:
Open Access publication

This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-ShareAlike 4.0 International
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 4.0 International