Virulence Factors from Pseudomonas aeruginosa Increase Lung Epithelial Permeability

Lung ◽  
2000 ◽  
Vol 178 (5) ◽  
pp. 261-269 ◽  
Author(s):  
A. O. Azghani ◽  
E. J. Miller ◽  
Barry T. Peterson
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Virulence Factors ◽  
Epithelial Permeability ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Asbestos-induced lung epithelial permeability: potential role of nonoxidant pathways

1998 ◽  
Vol 275 (2) ◽  
pp. L262-L268
Author(s):  
Michael W. Peterson ◽  
Jennifer Kirschbaum
Keyword(s):  
Tyrosine Kinase ◽  
Lung Fibrosis ◽  
Human Lung ◽  
Biological Effects ◽  
Tyrosine Phosphatase ◽  
Epithelial Permeability ◽  
Lung Epithelium ◽  
Asbestos Fibers ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Asbestos fibers are an important cause of lung fibrosis; however, the biological mechanisms are incompletely understood. The lung epithelium serves an important barrier function in the lung, and disrupting the epithelial barrier can contribute to lung fibrosis. Lung epithelial permeability is increased in patients with asbestosis, and asbestos fibers increase permeability across cultured human lung epithelium. However, the mechanism of this increased permeability is not known. Many of the biological effects of asbestos are postulated to be due to its ability to generate oxidants, and oxidants are known to increase epithelial permeability. However, we previously reported that altering the iron content of asbestos (important in oxidant generation) had no effect on its ability to increase permeability. For that reason, we undertook these studies to determine whether asbestos increases epithelial permeability through nonoxidant pathways. Both extracellular (H2O2) and intracellular (menadione) oxidants increase paracellular permeability across human lung epithelial monolayers. Extracellular catalase but not superoxide dismutase prevented increased permeability after both oxidant exposures. However, catalase offered no protection from asbestos-induced permeability. We next depleted the cells of glutathione or catalase to determine whether depleting normal cellular antioxidants would increase the sensitivity to asbestos. Permeability was the same in control cells and in cells depleted of these antioxidants. In addition to generating oxidants, asbestos also activates signal transduction pathways. Blocking protein kinase C activation did not prevent asbestos-induced permeability; however, blocking tyrosine kinase with tyrophostin A25 did prevent asbestos-induced permeability, and blocking tyrosine phosphatase with sodium vanadate enhanced the effect of asbestos. These data demonstrate that asbestos may increase epithelial permeability through nonoxidant pathways that involve tyrosine kinase activation. This model offers an important system for studying pathways involved in regulating lung epithelial permeability.

Lung epithelial permeability: relation to nonspecific airway responsiveness

1984 ◽  
Vol 57 (1) ◽  
pp. 77-84 ◽  
Author(s):  
P. M. O'Byrne ◽  
M. Dolovich ◽  
R. Dirks ◽  
R. S. Roberts ◽  
M. T. Newhouse
Keyword(s):  
Airway Responsiveness ◽  
Epithelial Permeability ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

The Effect of Ultrasonically Nebulized Distilled Water on Lung Epithelial Permeability

CHEST Journal ◽  
1983 ◽  
Vol 83 (6) ◽  
pp. 934-935 ◽  
Author(s):  
C.D. R. Borland ◽  
A.T. Chamberlain ◽  
T.W. Higenbottam
Keyword(s):  
Distilled Water ◽  
Epithelial Permeability ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

scholarly journals Increased claudin‐5 increases lung epithelial permeability and is associated with disruption of tight junction assembly

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Christian Overgaard ◽  
Leslie A. Mitchell ◽  
Christina Ward ◽  
David M. Guidot ◽  
Michael Koval
Keyword(s):  
Tight Junction ◽  
Epithelial Permeability ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Evaluation of lung epithelial permeability

1987 ◽  
Vol 13 (S1) ◽  
Author(s):  
MichaelI. Newhouse ◽  
Manel Jordana ◽  
Myrna Dolovich
Keyword(s):  
Epithelial Permeability ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Effects of platelet-activating factor on lung epithelial permeability in the guinea-pig

1991 ◽  
Vol 4 (4) ◽  
pp. 233-238 ◽  
Author(s):  
I. Macquin-Mavier ◽  
M.L. Franco-Montoya ◽  
J. Rosso ◽  
P.H. Jarreau ◽  
M. Meignan ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Platelet Activating Factor ◽  
Epithelial Permeability ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Lung epithelial permeability to aerosolized solutes: relation to position

1987 ◽  
Vol 62 (3) ◽  
pp. 902-911 ◽  
Author(s):  
M. Meignan ◽  
J. Rosso ◽  
R. Robert
Keyword(s):  
Left Lung ◽  
Normal Subjects ◽  
Aerosol Deposition ◽  
Gravity Gradient ◽  
Epithelial Permeability ◽  
Alveolar Volume ◽  
Lung Epithelial ◽  
Lateral Decubitus ◽  
Lung Epithelial Permeability ◽  
The Right

The lung epithelial permeability to inhaled solutes is primarily attributed to the degree of distension of the interepithelial junctions and thus of the alveolar volume. To assess this hypothesis, a submicronic aerosol of technetium-99m-labeled diethylenetriamine pentaacetate (99mTc-DTPA) was inhaled by eight normal subjects in left lateral decubitus (LLD). The regional lung clearance of 99mTc-DTPA was measured in LLD, then in right lateral decubitus (RLD) to reverse the relative distension of the alveoli. Although in LLD the deposition of the aerosol is the greatest in the gravity-dependent regions of the left lung, their 99mTc-DTPA clearances are significantly lower than those of the nondependent regions of the right lung (0.7 +/- 0.3 vs. 2 +/- 0.8%/min, P less than 0.001). In RLD, these regions placed in opposite positions significantly reversed their clearances (1.6 +/- 0.8 vs. 0.6 +/- 0.2%/min, P less than 0.001). Results indicate in lateral decubitus a gravity gradient of 99mTc-DTPA clearances independent of the aerosol deposition. This gradient of epithelial permeability to solutes appears to be influenced by the gradient of alveolar volume.

Asbestos directly increases lung epithelial permeability

1993 ◽  
Vol 265 (3) ◽  
pp. L308-L317 ◽  
Author(s):  
M. W. Peterson ◽  
M. E. Walter ◽  
T. J. Gross
Keyword(s):  
Recent Observation ◽  
Asbestos Exposure ◽  
Absolute Permeability ◽  
Epithelial Permeability ◽  
Chrysotile Asbestos ◽  
Direct Effects ◽  
Lactate Dehydrogenase Release ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability ◽  
Fibrotic Lung Disease

Asbestos causes the fibrotic lung disease asbestosis, but the biologic basis for this is unknown. Lung epithelial dysfunction including increased permeability is hypothesized to contribute to lung scarring in other forms of pulmonary fibrosis. Lung epithelial permeability is increased in both animals and humans exposed to asbestos. It is not known whether the increased epithelial permeability results from direct effects of asbestos or occurs as a result of the inflammatory reaction to asbestos fibers. To address this question we used a cultured human lung epithelial model, and we measured the direct effect of asbestos on lung epithelial barrier integrity as measured by mannitol permeability. We exposed the monolayer to chryogenically ground, respirable-sized chrysotile asbestos particles. This chrysotile asbestos caused a dose- and time-dependent increase in mannitol permeability across the epithelial monolayer. Increased mannitol permeability occurred both in the presence and in the absence of serum, was not due to cytotoxicity as measured by lactate dehydrogenase release, and was not associated with altered actin cytoskeleton at the light microscopic level. Permeability to 70 kDa neutral dextran also increased after asbestos exposure; however, the absolute permeability to dextran was less than mannitol permeability. Neither latex beads nor tantalum caused any change in permeability, suggesting that our findings are not explained by nonspecific effects of particles. Increased permeability did not reverse in the continued presence of asbestos and persisted even after removing the asbestos. Finally, surface-bound iron did not appear to be necessary for this effect because neither chelating iron with deferoxamine nor iron-loading the asbestos altered the effect on mannitol permeability. These results show that asbestos has direct effects on lung epithelial permeability. Together with the recent observation that asbestos directly increases epithelial fibrinolytic activity, our results suggest a novel mechanism for asbestos-induced lung injury.

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