The uptake of a Klebsiella pneumoniae capsule polysaccharide mutant triggers an inflammatory response by human airway epithelial cells

Internalization Cytochalasin D
DOI: 10.1099/mic.0.28285-0 Publication Date: 2006-01-25T06:22:47Z
ABSTRACT
The means by which airway epithelial cells sense a bacterial infection and intracellular signalling pathways are activated upon poorly understood. A549 human primary (NHBE) were used to investigate the response with Klebsiella pneumoniae. Infection of NHBE K. pneumoniae 52K10, capsule polysaccharide (CPS) mutant, increased surface levels ICAM-1 caused release IL-8. By contrast, wild-type strain did not elicit these responses. Consistent functional role for responses, there was correlation between number adherent leukocytes on cell surface. In addition, treatment neutrophils IL-8 enhanced their ability kill Strain 52K10 internalized more efficiently than wild-type, when infections performed in presence cytochalasin D inflammatory abrogated. These findings suggest that cellular activation is mediated internalization CPS prevents through blockage adhesion uptake. Collectively, results indicate could be triggering signal innate immune system airway. shown trigger nuclear translocation NF-kappaB. Evidence presented showing production Toll-like receptor (TLR) 2 TLR4 use soluble CD14 as TLR co-receptor.
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