Streptococcus mutans autolysin AtlA is a fibronectin-binding protein and contributes to bacterial survival in the bloodstream and virulence for infective endocarditis

Chiau Jing Jung, Quan H. Zheng, Ya Hsiung Shieh, Chi Shuan Lin, Jean S. Chia

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Streptococcus mutans, a commensal of the human oral cavity, can survive in the bloodstream and cause infective endocarditis (IE). However, the virulence factors associated with this manifestation of disease are not known. Here, we demonstrate that AtlA, an autolysin of S. mutans is a newly identified fibronectin (Fn) binding protein and contributes to bacterial resistance to phagocytosis and survival in the bloodstream. Interestingly, prior exposure to plasma at low concentrations was sufficient to enhance bacterial survival in the circulation. Calcium ions at physiological plasma concentrations induced maturation of AtlA from the 104-90 kDa isoform resulting in increased Fn binding and resistance to phagocytosis. An isogenic mutant strain defective in AtlA expression exhibited reduced survival and virulence when tested in a rat model of IE compared with the wild-type and complemented strains. The data presented suggest that plasma components utilized by S. mutans enhanced survival in the circulation and AtlA is a virulence factor associated with infective endocarditis.

Original languageEnglish
Pages (from-to)888-902
Number of pages15
JournalMolecular Microbiology
Volume74
Issue number4
DOIs
Publication statusPublished - Nov 2009
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Microbiology

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