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Type: Journal article
Title: The ClpP protease of Streptococcus pneumoniae modulates virulence gene expression and protects against fatal pneumococcal challenge
Author: Kwon, H.
Ogunniyi, A.
Choi, M.
Pyo, S.
Rhee, D.
Paton, J.
Citation: Infection and Immunity, 2004; 72(10):5646-5653
Publisher: Amer Soc Microbiology
Issue Date: 2004
ISSN: 0019-9567
Statement of
Hyog-Young Kwon, A. David Ogunniyi, Moo-Hyun Choi, Suhk-Neung Pyo, Dong-Kwon Rhee, and James C. Paton
Abstract: Streptococcus pneumoniae usually colonizes the nasopharynx of humans asymptomatically but occasionally translocates from this niche to the lungs, the brain, and the blood, causing potentially fatal infections. Spread to other host tissues requires a significant morphological change and the expression of virulence factors, such as capsular polysaccharide, and virulence proteins, such as pneumolysin (Ply), PspA, and CbpA. Modulation of the expression of pneumococcal virulence genes by heat shock and by heat shock proteins ClpL and ClpP, as well as the attenuation of virulence of a clpP mutant in a murine intraperitoneal infection model, was demonstrated previously. In this study, we further investigated the underlying mechanism of virulence attenuation by the clpP mutation. The half-lives of the mRNAs of ply and of the first gene of the serotype 2 capsule synthesis locus [cps(2)A] in the clpP mutant were more than twofold longer than those of the parent after heat shock, suggesting that the mRNA species were regulated posttranscriptionally by ClpP. In addition, the clpP mutant was defective in colonization of the nasopharynx and survival in the lungs of mice after intranasal challenge. The mutant was also killed faster than the parent in the murine macrophage RAW264.7 cell line, indicating that ClpP is required for colonization and intracellular survival in the host. Furthermore, fractionation studies demonstrated that ClpP was translocated into the cell wall after heat shock, and immunization of mice with ClpP elicited a protective immune response against fatal systemic challenge with S. pneumoniae D39, making ClpP a potential vaccine candidate for pneumococcal disease.
Keywords: Lung
Cell Line
Cell Wall
Mice, Inbred CBA
Streptococcus pneumoniae
Pneumococcal Infections
Endopeptidase Clp
Serine Endopeptidases
RNA, Messenger
Survival Rate
Gene Expression Regulation, Bacterial
RNA Stability
Heat-Shock Response
Adenosine Triphosphatases
Description: Copyright © 2004, American Society for Microbiology.
DOI: 10.1128/IAI.72.10.5646-5653.2004
Published version:
Appears in Collections:Aurora harvest 2
Molecular and Biomedical Science publications

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