The influence of polymorphonuclear leukocytes on altered pulmonary epithelial permeability during ozone exposure

Reinhart, Paul G.; Bassett, D. J. P.; Bhalla, Deepak K.

doi:10.1016/s0300-483x(98)00024-9

Cited by 14 publications

(5 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar findings were reported from O 3 -exposed mice genetically deficient in either one or both TNF receptors (TNFR1 and TNFR2) or mice treated with an IL-1 receptor antagonist before O 3 exposure (16,55). Because there is no distinction in the degree of lung permeability between wild-type and CXCR2-deficient mice, it is unlikely that the differences in the number of BALF neutrophils observed between genotypes contribute to this response, a finding consistent with other studies (41,57). Furthermore, reduced numbers of neutrophils in the air spaces have been associated with decreased epithelial cell sloughing (46).…”

Section: Discussionsupporting

confidence: 88%

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

Johnston¹,

Mizgerd²,

Shore³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

104

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 88%

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

Johnston¹,

Mizgerd²,

Shore³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

104

View full text Add to dashboard Cite

show abstract

“…• PMN influx and changes in epithelial permeability (as measured by protein in BAL) may not be mutually dependent events, which is in agreement with previous reports using other inhaled agents (Kleeberger and Hudak, 1992;Laughlin et al, 1986;Raj et al, 1985;Reinhart et al, 1998).…”

Section: Fig 4 Total Number Of Polymorphonuclear Leukocytes (Pmns) (A)supporting

confidence: 90%

Development of Pulmonary Tolerance in Mice Exposed to Zinc Oxide Fumes

Wesselkamper¹,

Chen²,

Gordon³

2001

Toxicological Sciences

View full text Add to dashboard Cite

As a result of repeated exposures to inhaled toxicants such as zinc oxide (ZnO), numerous individuals acquire tolerance to the exposures and display reduced symptoms. To ascertain whether tolerance is developed in an animal model, NIH-Swiss mice were exposed to 1.0 mg/m(3) ZnO for 1, 3, or 5 days (1X, 3X, or 5X), and polymorphonuclear leukocyte (PMN) and protein levels in bronchoalveolar lavage (BAL) were measured. Mice acquired tolerance to neutrophil infiltration into the lungs, as total PMNs returned near baseline in 5X-exposed animals as compared to that of the 1X exposure group (1X = 2.7 +/- 0.4 x 10(4), 5X = 0.2 +/- 0.1 x 10(4), mean +/- SE, p < 0.05). Development of tolerance to changes in lavageable protein, however, was not observed (1X = 313 +/- 29 microg/ml, 5X = 684 +/- 71 microg/ml, p < 0.05). Tolerance to PMN influx did not persist following re-exposure to ZnO after 5 days of rest. In contrast to ZnO exposure, following single and repeated exposure to aerosolized endotoxin there was development of tolerance to protein in BAL (1X = 174 +/- 71 microg/ml, 5X = 166 +/- 14 microg/ml, p > 0.05), but not to PMN influx (1X = 5.5 +/- 1.7 x 10(4), 13.9 +/- 1.7 x 10(4), p < 0.05). Induction of lung metallothionein (MT) was also observed in mice exposed once or repeatedly exposed to ZnO, suggesting that MT may play a role in its molecular mechanism.

show abstract

“…The apparent dissociation between inflammatory and hyperpermeability responses to O 3 has been suggested by a number of previous studies. For example, Reinhart et al (35) induced neutrophilic inflammation in rats (with 1% rabbit serum) before acute exposure to 0.8 ppm O 3 and found that enhanced neutrophilic infiltration did not augment the pulmonary hyperpermeability with inhaled O 3 . In another study, mice were treated with cyclophosphamide, colchicine, or indomethacin to inhibit or deplete neutrophils before acute exposure to 2 ppm O 3 , and all treatments had no effect on O 3 -induced lung hyperpermeability (17).…”

Section: Discussionmentioning

confidence: 99%

Ozone-induced lung inflammation and hyperreactivity are mediated via tumor necrosis factor-α receptors

Cho

Zhang

Kleeberger

2001

American Journal of Physiology-Lung Cellular and Molecular Phys

149

142

View full text Add to dashboard Cite

This study was designed to investigate the mechanisms through which tumor necrosis factor (Tnf) modulates ozone (O(3))-induced pulmonary injury in susceptible C57BL/6J (B6) mice. B6 [wild-type (wt)] mice and B6 mice with targeted disruption (knockout) of the genes for the p55 TNF receptor [TNFR1(-/-)], the p75 TNF receptor [TNFR2(-/-)], or both receptors [TNFR1/TNFR2(-/-)] were exposed to 0.3 parts/million O(3) for 48 h (subacute), and lung responses were determined by bronchoalveolar lavage. All TNFR(-/-) mice had significantly less O(3)-induced inflammation and epithelial damage but not lung hyperpermeability than wt mice. Compared with air-exposed control mice, O(3) elicited upregulation of lung TNFR1 and TNFR2 mRNAs in wt mice and downregulated TNFR1 and TNFR2 mRNAs in TNFR2(-/-) and TNFR1(-/-) mice, respectively. Airway hyperreactivity induced by acute O(3) exposure (2 parts/million for 3 h) was diminished in knockout mice compared with that in wt mice, although lung inflammation and permeability remained elevated. Results suggested a critical role for TNFR signaling in subacute O(3)-induced pulmonary epithelial injury and inflammation and in acute O(3)-induced airway hyperreactivity.

show abstract

The influence of polymorphonuclear leukocytes on altered pulmonary epithelial permeability during ozone exposure

Cited by 14 publications

References 20 publications

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

Development of Pulmonary Tolerance in Mice Exposed to Zinc Oxide Fumes

Ozone-induced lung inflammation and hyperreactivity are mediated via tumor necrosis factor-α receptors

Contact Info

Product

Resources

About