J Appl Biomed 8:131-140, 2010 | DOI: 10.2478/v10136-009-0016-6

Streptococcus pneumoniae: from molecular biology to host-pathogen interactions

Pedro García, Miriam Moscoso, Violeta Rodríguez-Cerrato, José Yuste, Ernesto García^*

Departamento de Microbiología Molecular y Biología de las Infecciones, Centro de Investigaciones Biológicas (CSIC), and CIBER de Enfermedades Respiratorias (CIBERES), Madrid, Spain

Streptococcus pneumoniae is the main cause of community acquired pneumonia and also produces meningitis, bacteremia, and otitis media, among others. Worldwide, these infections are the cause of substantial morbidity and mortality. Many different virulence factors have been described and most of them are surface-located macromolecules, namely, the capsular polysaccharide and various pneumococcal proteins. Cell wall hydrolases (CWHs) specifically cleave covalent bonds of the peptidoglycan and associated polymers: most CWHs are choline-binding proteins (CBPs) and are among the most well-known surface proteins. Pneumococcal CBPs have been investigated due to their role in pathogenesis and as candidate antigens for improved vaccines. Among the complex host-parasite interactions characteristic of pneumococcal disease, nasopharyngeal colonization is the first step. CBPs appear to play a central role in the development of the carrier state, possibly by affecting biofilm formation and development. Although the role of biofilms in the pathogenesis of some chronic human infections is currently widely accepted, the molecular bases underlying the formation of pneumococcal biofilms are only recently being studied. Among therapeutic strategies to combat multidrug-resistant pneumococcal infections, the use of purified phage- or bacteria-encoded CWHs both in vitro and in animal models is under investigation.

Keywords: Pneumococcus; cell wall hydrolases; choline; phage therapy; biofilm; enzybiotics

Received: February 23, 2010; Revised: April 8, 2010; Published: July 31, 2010  Show citation