Literature DB >> 8902481

Pseudomonas aeruginosa adherence to remodelling respiratory epithelium.

S de Bentzmann1, P Roger, E Puchelle.   

Abstract

Pseudomonas aeruginosa is an opportunistic organism, which frequently colonizes the respiratory tract of patients with impaired host defence. In cystic fibrosis (CF) patients, this pathogen causes a progressive destructive bronchitis and bronchiolitis and is responsible for high mortality. Normal respiratory epithelium is protected against bacteria via mucus and mucociliary clearance. Alteration of mucociliary clearance and of glycosylation of mucins in CF facilitates the access of bacteria to the underlying airway epithelial cells. Intact respiratory epithelium does not bind P. aeruginosa, whereas injured respiratory epithelium is highly susceptible to P. aeruginosa adherence. We found that the high affinity of respiratory epithelium, from CF and non-CF sources, for P. aeruginosa, during the wound repair process is related to the apical expression of asialo ganglioside M1 (aGM1). The affinity of repairing respiratory epithelium for P. aeruginosa is time-dependent, and is related to transient apical expression of aGM1 at the surface of repairing respiratory epithelial cells. CF respiratory epithelial cells apically express more aGM1 residues with relation to an increased affinity for P. aeruginosa than non CF cells. High epithelial damage followed by repair represents a major cause of P. aeruginosa adherence to airway epithelium in cystic fibrosis. However, P. aerurignosa adherence and colonization are not restricted to cystic fibrosis disease and P. aeruginosa pneumonia may also occur in severely immunocompromised patients, suggesting that epithelial injury and decreased host-response favour the colonization of the airways by P. aeruginosa.

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Year:  1996        PMID: 8902481     DOI: 10.1183/09031936.96.09102145

Source DB:  PubMed          Journal:  Eur Respir J        ISSN: 0903-1936            Impact factor:   16.671


  18 in total

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Journal:  Cell Microbiol       Date:  2010-03-12       Impact factor: 3.715

2.  Burkholderia cepacia produces a hemolysin that is capable of inducing apoptosis and degranulation of mammalian phagocytes.

Authors:  M L Hutchison; I R Poxton; J R Govan
Journal:  Infect Immun       Date:  1998-05       Impact factor: 3.441

3.  The phosphoinositol-3-kinase-protein kinase B/Akt pathway is critical for Pseudomonas aeruginosa strain PAK internalization.

Authors:  A Kierbel; A Gassama-Diagne; K Mostov; J N Engel
Journal:  Mol Biol Cell       Date:  2005-03-16       Impact factor: 4.138

4.  Modulation of cytosolic Ca(2+) concentration in airway epithelial cells by Pseudomonas aeruginosa.

Authors:  Tobias Jacob; Rebecca J Lee; Joanne N Engel; Terry E Machen
Journal:  Infect Immun       Date:  2002-11       Impact factor: 3.441

Review 5.  The epidemiology, pathogenesis and treatment of Pseudomonas aeruginosa infections.

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Review 6.  Receptor mimicry as novel therapeutic treatment for biothreat agents.

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7.  The ADP ribosyltransferase domain of Pseudomonas aeruginosa ExoT contributes to its biological activities.

Authors:  L Garrity-Ryan; S Shafikhani; P Balachandran; L Nguyen; J Oza; T Jakobsen; J Sargent; X Fang; S Cordwell; M A Matthay; J N Engel
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8.  Epithelial cell polarity alters Rho-GTPase responses to Pseudomonas aeruginosa.

Authors:  Barbara I Kazmierczak; Keith Mostov; Joanne N Engel
Journal:  Mol Biol Cell       Date:  2003-10-31       Impact factor: 4.138

Review 9.  Mimicking the host and its microenvironment in vitro for studying mucosal infections by Pseudomonas aeruginosa.

Authors:  Aurélie Crabbé; Maria A Ledesma; Cheryl A Nickerson
Journal:  Pathog Dis       Date:  2014-05-23       Impact factor: 3.166

10.  Subversion of mucosal barrier polarity by pseudomonas aeruginosa.

Authors:  Joanne Engel; Yonatan Eran
Journal:  Front Microbiol       Date:  2011-05-26       Impact factor: 5.640

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