Literature DB >> 2113073

Polymorphonuclear leukocyte- and Pseudomonas aeruginosa-induced damage to a human pulmonary epithelial cell line.

M M Dunn1, M Dunne, D W Kamp.   

Abstract

Polymorphonuclear leukocytes (PMNL) or Pseudomonas aeruginosa can damage the lung, but the manner in which they interact to induce toxicity is unclear. An in vitro model of the pulmonary epithelium was used to investigate interactions of PMNL and P. aeruginosa on epithelial cytotoxicity. A low inoculum of P. aeruginosa (10(7) bacteria) was minimally toxic to the epithelial cells (lysis = 9.0 +/- 2.9, detachment = 3.5 +/- 1.4). The addition of PMNL to the low inoculum markedly increased damage to the epithelial cells (lysis = 18.1 +/- 3.9, detachment = 17.6 +/- 3.6). Both the bacterium and a low-molecular-weight exoproduct were able to induce PMNL-mediated damage to epithelial cells. The damage was inhibited by serum or the addition of alpha 1 antiprotease but not by antioxidants. A larger inoculum of P. aeruginosa (10(9) bacteria) was directly toxic to the pulmonary cells (lysis = 44.8 +/- 4.1, detachment = 7.6 +/- 0.7). The damage was mediated by a heat-labile bacterial exoproduct. Pulmonary epithelial damage following pseudomonal infections may be related to either neutrophil or bacterial activity depending on the bacterial inoculum.

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Year:  1990        PMID: 2113073     DOI: 10.1093/infdis/162.1.172

Source DB:  PubMed          Journal:  J Infect Dis        ISSN: 0022-1899            Impact factor:   5.226


  8 in total

1.  Preliminary characterization of Pseudomonas aeruginosa peptide chemotactins for polymorphonuclear leukocytes.

Authors:  P A Fontán; C R Amura; V E García; M C Cerquetti; D O Sordelli
Journal:  Infect Immun       Date:  1992-06       Impact factor: 3.441

2.  Suppression of polymorphonuclear leucocyte chemotaxis by Pseudomonas aeruginosa elastase in vitro: a study of the mechanisms and the correlation with ring abscess in pseudomonal keratitis.

Authors:  Y Ijiri; K Matsumoto; R Kamata; N Nishino; R Okamura; T Kambara; T Yamamoto
Journal:  Int J Exp Pathol       Date:  1994-12       Impact factor: 1.925

3.  Alveolar response to Pseudomonas aeruginosa: role of the type III secretion system.

Authors:  F Ader; R Le Berre; K Faure; P Gosset; O Epaulard; B Toussaint; B Polack; E Nowak; N B Viget; E Kipnis; B P Guery
Journal:  Infect Immun       Date:  2005-07       Impact factor: 3.441

4.  Pseudomonas and neutrophil products modify transferrin and lactoferrin to create conditions that favor hydroxyl radical formation.

Authors:  B E Britigan; B L Edeker
Journal:  J Clin Invest       Date:  1991-10       Impact factor: 14.808

5.  Clindamycin, erythromycin, and roxithromycin inhibit the proinflammatory interactions of Pseudomonas aeruginosa pigments with human neutrophils in vitro.

Authors:  G J Ras; R Anderson; G W Taylor; J E Savage; E van Niekerk; G Joone; H J Koornhof; J Saunders; R Wilson; P J Cole
Journal:  Antimicrob Agents Chemother       Date:  1992-06       Impact factor: 5.191

6.  Protease-cleaved iron-transferrin augments oxidant-mediated endothelial cell injury via hydroxyl radical formation.

Authors:  R A Miller; B E Britigan
Journal:  J Clin Invest       Date:  1995-06       Impact factor: 14.808

7.  Protease cleavage of iron-transferrin augments pyocyanin-mediated endothelial cell injury via promotion of hydroxyl radical formation.

Authors:  R A Miller; G T Rasmussen; C D Cox; B E Britigan
Journal:  Infect Immun       Date:  1996-01       Impact factor: 3.441

8.  Bacterial toxin-induced pulmonary epithelial cytotoxicity and the protective effect of dibutyryl-cAMP.

Authors:  W Bourke; D Kamp; M Dunn; S W Chang
Journal:  Ir J Med Sci       Date:  1998 Jan-Mar       Impact factor: 2.089

  8 in total

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