Pneumococcal histidine triad proteins are regulated by the Zn2+-dependent repressor AdcR and inhibit complement deposition through the recruitment of complement factor H

Article


Ogunniyi, Abiodun D., Grabowicz, Marcin, Mahdi, Layla K., Cook, Jan, Gordon, David L., Sadlon, Tania A. and Paton, James C.. 2009. "Pneumococcal histidine triad proteins are regulated by the Zn2+-dependent repressor AdcR and inhibit complement deposition through the recruitment of complement factor H." The FASEB Journal. 23 (3), pp. 731-738. https://doi.org/10.1096/fj.08-119537
Article Title

Pneumococcal histidine triad proteins are regulated by the Zn2+-dependent repressor AdcR and inhibit complement deposition through the recruitment of complement factor H

ERA Journal ID2078
Article CategoryArticle
AuthorsOgunniyi, Abiodun D. (Author), Grabowicz, Marcin (Author), Mahdi, Layla K. (Author), Cook, Jan (Author), Gordon, David L. (Author), Sadlon, Tania A. (Author) and Paton, James C. (Author)
Journal TitleThe FASEB Journal
Journal Citation23 (3), pp. 731-738
Number of Pages8
Year2009
Place of PublicationUnited States
ISSN0892-6638
1530-6860
Digital Object Identifier (DOI)https://doi.org/10.1096/fj.08-119537
Web Address (URL)https://www.fasebj.org/doi/10.1096/fj.08-119537
Abstract

The pneumococcal histidine triad (Pht) proteins are a recently recognized family of surface proteins, comprising 4 members: PhtA, PhtB, PhtD, and PhtE. They are being promoted for inclusion in a multicomponent pneumococcal protein vaccine currently under development, but to date, their biological functions and their relative contributions to pathogenesis have not been clarified. In this study, the involvement of these proteins in pneumococcal virulence was investigated in murine models of sepsis and pneumonia by using defined, nonpolar mutants of the respective genes in Streptococcus pneumoniae D39. In either challenge model, mutagenesis of all 4 genes was required to completely abolish virulence relative to the wild-type, suggesting significant functional redundancy among Pht proteins. The in vivo expression of pht genes was significantly up- regulated in the nasopharynx and lungs compared with blood. We provide unequivocal molecular evidence for Zn2+-dependent, AdcR-mediated, regulation of pht gene expression by real-time reverse transcriptase-polymerase chain reaction, Western blotting, and electrophoretic mobility-shift assays. We also present the first direct evidence for the biological function of this protein family by demonstrating that Pht proteins are required for inhibition of complement deposition on the pneumococcal surface through the recruitment of complement factor H.

KeywordsStreptococcus pneumonia; virulence; gene expression, innate immunity; protein vaccines
ANZSRC Field of Research 2020310701. Bacteriology
320405. Humoural immunology and immunochemistry
320701. Medical bacteriology
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Byline AffiliationsUniversity of Adelaide
Flinders University
Institution of OriginUniversity of Southern Queensland
Funding source
NHMRC
Grant ID
284214
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