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Crude 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 Cells

Title
Crude 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 Cells
Authors
Ko, Su HyukRho, Da JeongJeon, Jong IkKim, Young-JeonWoo, Hyun AeKim, NayoungKim, Jung Mogg
Ewha Authors
우현애
SCOPUS Author ID
우현애scopus
Issue Date
2016
Journal Title
INFECTION AND IMMUNITY
ISSN
0019-9567JCR Link1098-5522JCR Link
Citation
vol. 84, no. 8, pp. 2162 - 2174
Publisher
AMER SOC MICROBIOLOGY
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Helicobacter 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.
DOI
10.1128/IAI.00190-16
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약학대학 > 약학과 > Journal papers
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