Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takenaka, R.
Right arrow Articles by Oguma, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takenaka, R.
Right arrow Articles by Oguma, K.
Agricola
Right arrow Articles by Takenaka, R.
Right arrow Articles by Oguma, K.
Microbiology 150 (2004), 3913-3922; DOI  10.1099/mic.0.27527-0
© 2004 Society for General Microbiology

Helicobacter pylori heat-shock protein 60 induces inflammatory responses through the Toll-like receptor-triggered pathway in cultured human gastric epithelial cells

Ryuta Takenaka1, Kenji Yokota2, Kiyoshi Ayada2, Motowo Mizuno1, Ying Zhao2, Yoshihito Fujinami2, Song-Nan Lin2, Tatsuya Toyokawa1, Hiroyuki Okada1, Yasushi Shiratori1 and Keiji Oguma2

1 Department of Medicine and Medical Science (Medicine 1), Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan
2 Department of Bacteriology, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan

Correspondence
Kenji Yokota
yokochan{at}md.okayama-u.ac.jp

Contact between Helicobacter pylori and gastric epithelial cells results in activation of NF-{kappa}B followed by secretion of interleukin (IL)-8. However, host-cell receptor(s) and their ligands involved in H. pylori-related IL-8 production have yet to be fully defined. In this study, the interaction between Toll-like receptors (TLRs), which are host receptors for pathogens involved in the innate immune response, and heat-shock protein (HSP) 60, an immune-potent antigen of H. pylori, was examined during H. pylori-induced IL-8 secretion in vitro. Recombinant H. pylori HSP60 (rHpHSP60) was prepared and added to cultured KATO III human gastric epithelial cells with or without pre-incubation with mouse monoclonal anti-TLR2 or anti-TLR4 antibodies. IL-8 mRNA expression and IL-8 protein release were analysed by Northern blotting and immunoassay. Involvement of NF-{kappa}B activation was analysed immunocytochemically by anti-NF-{kappa}B p65 antibody and ammonium pyrrolidinedithiocarbamate (PDTC), an inhibitor of NF-{kappa}B-mediated transcriptional activation. rHpHSP60 induced IL-8 mRNA expression and IL-8 secretion in a dose-dependent manner in KATO III cells. Anti-TLR2 antibody inhibited rHpHSP60-induced IL-8 secretion by 75 %, and anti-TLR4 antibody inhibited it by 30 %. rHpHSP60 induced nuclear translocation of NF-{kappa}B p65, which was inhibited by pretreatment with anti-TLR2 antibody. Treatment with PDTC significantly decreased the secretion of IL-8 induced by rHpHSP60. These findings suggest that H. pylori HSP60 activates NF-{kappa}B and induces IL-8 production through TLR-triggered pathways in gastric epithelial cells. Thus, it is possible that H. pylori HSP60 and TLR interaction in host cells contributes to the development of gastric inflammation caused by H. pylori infection.

Abbreviations: FCS, fetal calf serum; G3PDH, glyceraldehyde-3-phosphate dehydrogenase; HSP, heat-shock protein; IL, interleukin; PDTC, ammonium pyrrolidinedithiocarbamate; PMB, polymyxin B; rHpHSP60, recombinant H. pylori HSP60; TLR, toll-like receptor; TNF-{alpha}, tumour necrosis factor {alpha}




This article has been cited by other articles:


Home page
 Ann OncolHome page
P. Adam, B. Schmausser, M. Gobeler-Kolve, H. K. Muller-Hermelink, and M. Eck
Gastric extranodal marginal zone B-cell lymphomas of MALT type exclusively express toll-like receptor 4 in contrast to other lymphomas infiltrating the stomach
Ann. Onc., March 1, 2008; 19(3): 566 - 569.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Thakran, H. Li, C. L. Lavine, M. A. Miller, J. E. Bina, X. R. Bina, and F. Re
Identification of Francisella tularensis Lipoproteins That Stimulate the Toll-like Receptor (TLR) 2/TLR1 Heterodimer
J. Biol. Chem., February 15, 2008; 283(7): 3751 - 3760.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
H. Gradisar, M. M. Keber, P. Pristovsek, and R. Jerala
MD-2 as the target of curcumin in the inhibition of response to LPS
J. Leukoc. Biol., October 1, 2007; 82(4): 968 - 974.
[Abstract] [Full Text] [PDF]

Home page
 J Med MicrobiolHome page
Y. Zhao, K. Yokota, K. Ayada, Y. Yamamoto, T. Okada, L. Shen, and K. Oguma
Helicobacter pylori heat-shock protein 60 induces interleukin-8 via a Toll-like receptor (TLR)2 and mitogen-activated protein (MAP) kinase pathway in human monocytes
J. Med. Microbiol., February 1, 2007; 56(2): 154 - 164.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Microbiol. Rev.Home page
H. M. S. Algood and T. L. Cover
Helicobacter pylori Persistence: an Overview of Interactions between H. pylori and Host Immune Defenses
Clin. Microbiol. Rev., October 1, 2006; 19(4): 597 - 613.
[Abstract] [Full Text] [PDF]

Home page
 J Med MicrobiolHome page
S.-N. Lin, K. Ayada, Y. Zhao, K. Yokota, R. Takenaka, H. Okada, R. Kan, S. Hayashi, M. Mizuno, Y. Hirai, et al.
Helicobacter pylori heat-shock protein 60 induces production of the pro-inflammatory cytokine IL8 in monocytic cells
J. Med. Microbiol., March 1, 2005; 54(3): 225 - 233.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2004 Society for General Microbiology.