Helicobacter pylori-derived outer membrane vesicles stimulate interleukin 8 secretion through nuclear factor kappa B activationopen access
- Authors
- Choi, Mun Sun; Ze, Eun Young; Park, Jae Yong; Shin, Tae-Seop; Kim, Jae Gyu
- Issue Date
- Jul-2021
- Publisher
- 대한내과학회
- Keywords
- Helicobacter pylori; Extracellular vesicles; Bacterial outer membrane proteins; Interleukin-8; NF-kappa B
- Citation
- The Korean Journal of Internal Medicine, v.36, no.4, pp 857 - 867
- Pages
- 11
- Journal Title
- The Korean Journal of Internal Medicine
- Volume
- 36
- Number
- 4
- Start Page
- 857
- End Page
- 867
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/50476
- DOI
- 10.3904/kjim.2019.432
- ISSN
- 1226-3303
2005-6648
- Abstract
- Background/Aims: Bacteria-derived outer membrane vesicles (OMVs) are commonly associated with various biological activities and functions. Helicobacter pylori- derived OMVs are thought to contribute to pathogenesis. This study aimed to investigate the effects of H. pylori-derived OMVs.
Methods: H. pylori strains were isolated from patients with gastritis, gastric ulcer, or gastric cancer using endoscopic biopsy. The U-937, AGS, and MKN-45 cell lines were exposed to H. pylori and H. pylori-derived OMVs. The expression of interleukin 8 (IL-8) messenger RNA (mRNA) was assessed using reverse transcription- polymerase chain reaction (RT-PCR) and real-time RT-PCR, and IL-8 secretion was analyzed using enzyme-linked immunosorbent assay. Nuclear factor kappa B (NF-κB) activation was evaluated by Western blotting.
Results: H. pylori and H. pylori-derived OMVs induced the expression of IL-8 mRNA and protein. Importantly, the bacteria induced higher IL-8 mRNA and protein expression than the OMVs. IL-8 expression was induced to different levels in response to H. pylori-derived OMVs from hosts with different gastric diseases.
Western blotting revealed the increased phosphorylation and reduced degradation of inhibitor of NF-κB alpha in cells exposed to OMVs.
Conclusions: H. pylori-derived OMVs may aid the development of various gastric diseases by inducing IL-8 production and NF-κB activation.
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