Journal
VIRULENCE
Volume 5, Issue 6, Pages 673-679Publisher
LANDES BIOSCIENCE
DOI: 10.4161/viru.32076
Keywords
sialic acid; K. pneumoniae; hypermucoviscosity; neutrophil; phagocytosis
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Funding
- Ministry of Science and Technology of Taiwan [MOST 100-2314-B-182A-026, 100-2314-B-758-001, 101-2314-B-182A-061-MY3]
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Klebsiella pneumoniae (KP) with the hypermucoviscosity (HV) phenotype has abundant capsular polysaccharides (CPS) and usually causes an invasive syndrome. Sialic acid (Sia), a component of CPS in KP strains with the HV phenotype, may be anti-phagocytic. Sia-binding immunoglobulin-like lectin-9 (Siglec-9) act as an MHC class-I receptor on neutrophils that recognizes Sia and sends a signal to dampen inflammatory response. Three clinical KP strains with KP-M1 (HV-positive; capsular serotype K-1), KP-14 (HV-negative; capsular serotype non-K-1/K-2), and DT-X (HV-negative; capsular serotype K-1) were studied. We assessed total Sia in CPS extracts using enzymatic methods and phagocytosis by neutrophils of neuraminidase-treated bacteria using flow cytometry. Neutrophil killing was evaluated in the presence and absence of antibodies against Siglec-9. The concentration of Sia was significantly higher in the CPS extract of KP-M1 (56.75 +/- 6.75 mu mole/10(9) cfu) than in the CPS extract of KP-14 (0.02 +/- 0.01 mu mole/109 cfu) and DT-X (a negligible value). The KP-M1 (compared with the KP-14 and DT-X) was more resistant to neutrophil phagocytosis. Both the HV phenotype and resistance to phagocytosis of KP-M1 were significantly decreased after Sia removal with neuraminidase treatment. Fluorescence microscopy with an antibody against human Siglec-9 showed attachment of KP-M1 (but were absent of KP-14 and DT-X) to the surface of neutrophils and colocalization with human Siglec-9. Engagement of Siglec-9 via Sia enhanced neutrophils killing of KP-M1 by ex vivo human neutrophils bactericidal activity assay. The result showed that Sia might be a constituent of KP-M1 CPS responsible for HV, thereby contributing to anti-phagocytic activity of this pathogen.
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