The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells

ABSTRACT In order for the opportunistic Gram-negative pathogen Pseudomonas aeruginosa to cause an airway infection, the pathogen interacts with epithelial cells and the overlying mucous layer. We examined the contribution of the biofilm polysaccharide Psl to epithelial cell adherence and the impact...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Matthew S. Byrd, Bing Pang, Meenu Mishra, W. Edward Swords, Daniel J. Wozniak
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2010
Materias:	Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/3b4da8ce0fd5412d9ac809ccce572402
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:3b4da8ce0fd5412d9ac809ccce572402
record_format	dspace
spelling	oai:doaj.org-article:3b4da8ce0fd5412d9ac809ccce5724022021-11-15T15:38:16ZThe <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells10.1128/mBio.00140-102150-7511https://doaj.org/article/3b4da8ce0fd5412d9ac809ccce5724022010-08-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.00140-10https://doaj.org/toc/2150-7511ABSTRACT In order for the opportunistic Gram-negative pathogen Pseudomonas aeruginosa to cause an airway infection, the pathogen interacts with epithelial cells and the overlying mucous layer. We examined the contribution of the biofilm polysaccharide Psl to epithelial cell adherence and the impact of Psl on proinflammatory signaling by flagellin. Psl has been implicated in the initial attachment of P. aeruginosa to biotic and abiotic surfaces, but its direct role in pathogenesis has not been evaluated (L. Ma, K. D. Jackson, R. M. Landry, M. R. Parsek, and D. J. Wozniak, J. Bacteriol. 188:8213–8221, 2006). Using an NF-κB luciferase reporter system in the human epithelial cell line A549, we show that both Psl and flagellin are necessary for full activation of NF-κB and production of the interleukin 8 (IL-8) chemokine. We demonstrate that Psl does not directly stimulate NF-κB activity, but indirectly as a result of increasing contact between bacterial cells and epithelial cells, it facilitates flagellin-mediated proinflammatory signaling. We confirm differential adherence of Psl and/or flagellin mutants by scanning electron microscopy and identify Psl-dependent membrane structures that may participate in adherence. Although we hypothesized that Psl would protect P. aeruginosa from recognition by the epithelial cell line A549, we instead observed a positive role for Psl in flagellin-mediated NF-κB activation, likely as a result of increasing contact between bacterial cells and epithelial cells. IMPORTANCE Pseudomonas aeruginosa is the predominant airway pathogen causing morbidity and mortality in individuals affected by the genetic disease cystic fibrosis. P. aeruginosa can also cause severe pneumonia, burn wound infections, and sepsis, making its overall impact on human health significant. The attachment of P. aeruginosa to host tissues, often leading to recalcitrant biofilm infections, and inflammation induced by flagellin are both important mechanisms of virulence. We explored the role of the biofilm polysaccharide Psl in the pathogenesis of P. aeruginosa and found that Psl is required for surface adherence to A549 epithelial cells, and as an adhesin, it facilitates flagellin-mediated NF-κB activation. This work was done to better understand the initial events of infection and revealed that a biofilm polysaccharide contributes to inflammation in a novel manner.Matthew S. ByrdBing PangMeenu MishraW. Edward SwordsDaniel J. WozniakAmerican Society for MicrobiologyarticleMicrobiologyQR1-502ENmBio, Vol 1, Iss 3 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Microbiology QR1-502
spellingShingle	Microbiology QR1-502 Matthew S. Byrd Bing Pang Meenu Mishra W. Edward Swords Daniel J. Wozniak The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells
description	ABSTRACT In order for the opportunistic Gram-negative pathogen Pseudomonas aeruginosa to cause an airway infection, the pathogen interacts with epithelial cells and the overlying mucous layer. We examined the contribution of the biofilm polysaccharide Psl to epithelial cell adherence and the impact of Psl on proinflammatory signaling by flagellin. Psl has been implicated in the initial attachment of P. aeruginosa to biotic and abiotic surfaces, but its direct role in pathogenesis has not been evaluated (L. Ma, K. D. Jackson, R. M. Landry, M. R. Parsek, and D. J. Wozniak, J. Bacteriol. 188:8213–8221, 2006). Using an NF-κB luciferase reporter system in the human epithelial cell line A549, we show that both Psl and flagellin are necessary for full activation of NF-κB and production of the interleukin 8 (IL-8) chemokine. We demonstrate that Psl does not directly stimulate NF-κB activity, but indirectly as a result of increasing contact between bacterial cells and epithelial cells, it facilitates flagellin-mediated proinflammatory signaling. We confirm differential adherence of Psl and/or flagellin mutants by scanning electron microscopy and identify Psl-dependent membrane structures that may participate in adherence. Although we hypothesized that Psl would protect P. aeruginosa from recognition by the epithelial cell line A549, we instead observed a positive role for Psl in flagellin-mediated NF-κB activation, likely as a result of increasing contact between bacterial cells and epithelial cells. IMPORTANCE Pseudomonas aeruginosa is the predominant airway pathogen causing morbidity and mortality in individuals affected by the genetic disease cystic fibrosis. P. aeruginosa can also cause severe pneumonia, burn wound infections, and sepsis, making its overall impact on human health significant. The attachment of P. aeruginosa to host tissues, often leading to recalcitrant biofilm infections, and inflammation induced by flagellin are both important mechanisms of virulence. We explored the role of the biofilm polysaccharide Psl in the pathogenesis of P. aeruginosa and found that Psl is required for surface adherence to A549 epithelial cells, and as an adhesin, it facilitates flagellin-mediated NF-κB activation. This work was done to better understand the initial events of infection and revealed that a biofilm polysaccharide contributes to inflammation in a novel manner.
format	article
author	Matthew S. Byrd Bing Pang Meenu Mishra W. Edward Swords Daniel J. Wozniak
author_facet	Matthew S. Byrd Bing Pang Meenu Mishra W. Edward Swords Daniel J. Wozniak
author_sort	Matthew S. Byrd
title	The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells
title_short	The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells
title_full	The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells
title_fullStr	The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells
title_full_unstemmed	The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells
title_sort	<italic toggle="yes">pseudomonas aeruginosa</italic> exopolysaccharide psl facilitates surface adherence and nf-κb activation in a549 cells
publisher	American Society for Microbiology
publishDate	2010
url	https://doaj.org/article/3b4da8ce0fd5412d9ac809ccce572402
work_keys_str_mv	AT matthewsbyrd theitalictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT bingpang theitalictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT meenumishra theitalictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT wedwardswords theitalictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT danieljwozniak theitalictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT matthewsbyrd italictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT bingpang italictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT meenumishra italictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT wedwardswords italictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells AT danieljwozniak italictoggleyespseudomonasaeruginosaitalicexopolysaccharidepslfacilitatessurfaceadherenceandnfkbactivationina549cells
_version_	1718427819495653376

The <italic toggle="yes">Pseudomonas aeruginosa</italic> Exopolysaccharide Psl Facilitates Surface Adherence and NF-κB Activation in A549 Cells

Ejemplares similares