Induction of gamma interferon and nitric oxide by truncated pneumolysin that lacks pore-forming activity

Baba, Hisashi, Kawamura, Ikuo, Kohda, Chikara, Nomura, Takamasa, Ito, Yutaka, Kimoto, Terumi, Watanabe, Isao, Ichiyama, Satoshi and Mitsuyama, Masao (2007) Induction of gamma interferon and nitric oxide by truncated pneumolysin that lacks pore-forming activity. Infection and Immunity, 70 1: 107-113. doi:10.1128/IAI.70.1.107-113.2002

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Author Baba, Hisashi
Kawamura, Ikuo
Kohda, Chikara
Nomura, Takamasa
Ito, Yutaka
Kimoto, Terumi
Watanabe, Isao
Ichiyama, Satoshi
Mitsuyama, Masao
Title Induction of gamma interferon and nitric oxide by truncated pneumolysin that lacks pore-forming activity
Journal name Infection and Immunity   Check publisher's open access policy
ISSN 1098-5522
1070-6313
Publication date 2007-01
Sub-type Article (original research)
DOI 10.1128/IAI.70.1.107-113.2002
Open Access Status File (Publisher version)
Volume 70
Issue 1
Start page 107
End page 113
Total pages 7
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Formatted abstract
Pneumolysin (PLY), an important virulence factor of Streptococcus pneumoniae, is known to exert various effects on the host immune cells, including cytokine induction, in addition to its known cytolytic activity as a member of the thiol-activated cytolysins. It is of interest to determine whether cytolytic activity is involved in triggering the cytokine production. In this study, we constructed full-length recombinant PLY and noncytolytic truncated PLYs with C-terminal deletions to examine the response of spleen cells to these PLY preparations. When cytolytic activity was blocked by treatment with cholesterol, full-length PLY was capable of inducing gamma interferon (IFN-γ) production. Truncated PLYs that originally exhibited no cytolytic activity were also active in IFN-γ induction. Therefore, the IFNγ inducing ability of PLY appeared to be independent of the cytolytic activity. Furthermore, IFNγinducing preparations were also capable of inducing nitric oxide synthase expression and nitric oxide (NO) production, and the addition of neutralizing antibody to IFNγ abolished the NO production. These results clearly demonstrated that PLY is capable of inducing IFN-γ production in spleen cells by a mechanism different from pore formation and that the induced IFN-γ stimulates NO production. These findings were discussed with reference to the contribution of PLY to the virulence of S. pneumoniae in vivo.

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Q-Index Status Provisional Code
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Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
 
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Created: Wed, 08 Apr 2009, 15:26:39 EST by Maryanne Watson on behalf of Anaesthesiology and Critical Care - RBWH