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The effect of alginate on the invasion of cystic fibrosis respiratory epithelial cells by clinical isolates of pseudomonas aeruginosa.

Authors
Massengale-ARD; Quinn-FJ; Williams-A; Gallagher-S; Aronoff-SC
Source
Exp Lung Res 2000 Apr-May; 26(3):163-178
NIOSHTIC No.
20032738
Abstract
Chronic infection in the cystic fibrosis (CF) lung is characterized by Pseudomonas aeruginosa strains that overproduce the mucoid exopolysaccharide, alginate. Previous experiments have shown that long-term survival of P. aeruginosa in the CF lung may be facilitated by increased adherence and decreased invasion of respiratory epithelial cells. Therefore, mucoid and nonmucoid clinical isolates of P. aeruginosa were assayed for their ability to associate with and invade the CF respiratory epithelial cell line, CF/T43 Association assays and gentamicin exclusion assays demonstrated that mucoid P. aeruginosa associates with and invades CF/T43 cell monolayers significantly less than nonmucoid P. aeruginosa strains (P =.004,.02). Fluorescence microscopy invasion assays confirmed these results. The differences in association and invasion by the P. aeruginosa strains were not due to differences in lipopolysaccharide phenotype or cytotoxicity for CF/T43 respiratory epithelial cells. Exogenous bacterial alginate had no effect on the invasion of CF respiratory epithelia by a nonmucoid strain. Invasion assays with the wild-type P. aeruginosa strain PAO1 end isogenic algU end mucA mutant strains failed to show differences in invasion (P = .25). We conclude that (i) mucoid P. aeruginosa isolates associate with and invade CF/T43 respiratory epithelial cells with less efficiency than nonmucoid P, aeruginosa, (ii) these differences are not due to variations in lipopolysaccharide phenotype between strains, (iii) neither exogenous nor endogenous alginate affects the ability of P, aeruginosa to invade CF/T43 respiratory epithelial cells, and (iv) invasion of CF/T43 respiratory epithelial cells by a laboratory reference strain of P. aeruginosa does not appear to be regulated by AlgU.
Keywords
Bacterial-disease; Bacterial-infections; Cell-biology; Cell-function; Cell-metabolism; Cellular-reactions; Cellular-uptake; Cellular-transport-mechanism; Respiratory-infections; Respiratory-system-disorders; Breathing; Pulmonary-system-disorders; Pulmonary-function
CODEN
EXLRDA
Publication Date
20000401
Document Type
Journal Article
Email Address
sby5@cdc.gov
Fiscal Year
2000
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
0190-2148
NIOSH Division
HELD
Source Name
Experimental Lung Research
State
WV; CT; MD
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