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 ID	2078
Article Category	Article
Authors	Ogunniyi, 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 Title	The FASEB Journal
Journal Citation	23 (3), pp. 731-738
Number of Pages	8
Year	2009
Place of Publication	United States
ISSN	0892-6638
	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.
Keywords	Streptococcus pneumonia; virulence; gene expression, innate immunity; protein vaccines
ANZSRC Field of Research 2020	310701. Bacteriology
	320405. Humoural immunology and immunochemistry
	320701. Medical bacteriology
Public Notes	Files associated with this item cannot be displayed due to copyright restrictions.
Byline Affiliations	University of Adelaide
	Flinders University
Institution of Origin	University of Southern Queensland
Funding source	NHMRC Grant ID 284214

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