PspK of Streptococcus pneumoniae increases adherence to epithelial cells and enhances nasopharyngeal colonization.
Infect Immun
; 81(1): 173-81, 2013 Jan.
Article
em En
| MEDLINE
| ID: mdl-23115034
ABSTRACT
Streptococcus pneumoniae (the pneumococcus) colonizes the human nasopharynx and can cause invasive disease aided by the pneumococcal capsule. Group II nontypeable S. pneumoniae (NTSp) lacks a polysaccharide capsule, and a subgroup of NTSp carriage isolates has been found to have a novel gene, pneumococcal surface protein K (pspK), which replaces the capsule locus. A recent rise in the number of NTSp isolates colonizing the human nasopharynx has been observed, but the colonization factors of NTSp have not been well studied. PspK has been shown to play a role in mouse colonization. We therefore examined PspK-mediated immune evasion along with adherence to host cells and colonization. PspK bound human secretory immunoglobulin A (sIgA) but not the complement regulator factor H and did not decrease C3b deposition on the pneumococcal surface. PspK increased binding of pneumococci to epithelial cells and enhanced pneumococcal colonization independently of the genetic background. Understanding how NTSp colonizes and survives within the nasopharynx is important due to the increase in NTSp carriage. Our data suggest that PspK may aid in the persistence of NTSp within the nasopharynx but is not involved in invasion.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Infecções Pneumocócicas
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Streptococcus pneumoniae
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Proteínas de Bactérias
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Aderência Bacteriana
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Nasofaringe
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Infect Immun
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
Estados Unidos