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PMID: 11580843 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

The pavA gene of Streptococcus pneumoniae encodes a fibronectin-binding protein that is essential for virulence.

Molecular microbiology ·Vol. 41 ·No. 6 ·2001-09-00 ·Pages 1395-408

Holmes AR, McNab R, Millsap KW, Rohde M, Hammerschmidt S, Mawdsley JL, Jenkinson HF

Abstract

Streptococcus pneumoniae colonizes the nasopharynx in up to 40% of healthy subjects, and is a leading cause of middle ear infections (otitis media), meningitis and pneumonia. Pneumococci adhere to glycosidic receptors on epithelial cells and to immobilized fibronectin, but the bacterial adhesins mediating these reactions are largely uncharacterized. In this report we describe a novel pneumococcal protein PavA, which binds fibronectin and is associated with pneumococcal adhesion and virulence. The pavA gene, present in 64 independent isolates of S. pneumoniae tested, encodes a 551 amino acid residue polypeptide with 67% identical amino acid sequence to Fbp54 protein in Streptococcus pyogenes. PavA localized to the pneumococcal cell outer surface, as demonstrated by immunoelectron microscopy, despite lack of conventional secretory or cell-surface anchorage signals within the primary sequence. Full-length recombinant PavA polypeptide bound to immobilized human fibronectin in preference to fluid-phase fibronectin, in a heparin-sensitive interaction, and blocked binding of wild-type pneumococcal cells to fibronectin. However, a C-terminally truncated PavA' polypeptide (362 aa residues) failed to bind fibronectin or block pneumococcal cell adhesion. Expression of pavA in Enterococcus faecalis JH2-2 conferred > sixfold increased cell adhesion levels to fibronectin over control JH2-2 cells. Isogenic mutants of S. pneumoniae, either abrogated in PavA expression or producing a 42 kDa C-terminally truncated protein, showed up to 50% reduced binding to immobilized fibronectin. Inactivation of pavA had no effects on growth rate, cell morphology, cell-surface physico-chemical properties, production of pneumolysin, autolysin, or surface proteins PspA and PsaA. Isogenic pavA mutants of encapsulated S. pneumoniae D39 were approximately 104-fold attenuated in virulence in the mouse sepsis model. These results provide evidence that PavA fibronectin-binding protein plays a direct role in the pathogenesis of pneumococcal infections.

MeSH Terms
Adhesins, Bacterial Animals Bacterial Adhesion Bacterial Outer Membrane Proteins/genetics,metabolism Bacterial Proteins/genetics,metabolism Base Sequence Carrier Proteins/genetics,metabolism DNA Primers/genetics DNA, Bacterial/genetics Fibronectins Gene Expression Genes, Bacterial Humans Mice Mice, Inbred BALB C Microscopy, Immunoelectron Pneumococcal Infections/etiology Sepsis/etiology Streptococcus pneumoniae/genetics,metabolism,pathogenicity,ultrastructure Virulence/genetics,physiology
Chemicals
Adhesins, Bacterial Bacterial Outer Membrane Proteins Bacterial Proteins Carrier Proteins DNA Primers DNA, Bacterial Fibronectins fibronectin-binding proteins, bacterial
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Holmes A R
Department of Oral Sciences and Orthodontics, University of Otago, Dunedin, New Zealand.
McNab R
Millsap K W
Rohde M
Hammerschmidt S
Mawdsley J L
Jenkinson H F
Article Info
Journal
Molecular microbiology
Abbr.
Mol Microbiol
ISSN
0950-382X
Published
2001-09-00
Pages
1395-408
Language
English
Region
England
NLM ID
8712028
Subset
IM
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