Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice

Nicholas Kenyon, Albert Van Der Vliet, Bettina C. Schock, Tatsuya Okamoto, Gabrielle M. McGrew, Jerold A Last

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

Mice deficient in inducible nitric oxide synthase (iNOS; C57B1/6Ai-[KO]NOS2 N5) or wild-type C57B1/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclear leukocytes. The iNOS knockout mice showed significantly greater levels of lung injury by all of these criteria than did the wild-type mice. We conclude that iNOS knockout mice are more susceptible to acute lung damage induced by exposure to ozone than are wild-type C57B1/6 mice and that protein nitration is associated with the degree of inflammation and not dependent on iNOS-derived nitric oxide.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume282
Issue number3 26-3
StatePublished - 2002

Fingerprint

Acute Lung Injury
Ozone
Chemokine CXCL2
Matrix Metalloproteinase 9
Knockout Mice
Lung
Proteins
Therapeutic Irrigation
Lung Injury
Nitric Oxide Synthase Type II
Tyrosine
Edema
Nitric Oxide
Neutrophils
Air
Inflammation

Keywords

  • Inflammation
  • Macrophage inflammatory protein-2
  • Matrix metalloproteinase-9
  • Nitric oxide
  • Nitrotyrosine

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology

Cite this

Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice. / Kenyon, Nicholas; Van Der Vliet, Albert; Schock, Bettina C.; Okamoto, Tatsuya; McGrew, Gabrielle M.; Last, Jerold A.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 282, No. 3 26-3, 2002.

Research output: Contribution to journalArticle

Kenyon, Nicholas ; Van Der Vliet, Albert ; Schock, Bettina C. ; Okamoto, Tatsuya ; McGrew, Gabrielle M. ; Last, Jerold A. / Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2002 ; Vol. 282, No. 3 26-3.
@article{983f7a670e3a404f9cc45b1ed18e2e22,
title = "Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice",
abstract = "Mice deficient in inducible nitric oxide synthase (iNOS; C57B1/6Ai-[KO]NOS2 N5) or wild-type C57B1/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclear leukocytes. The iNOS knockout mice showed significantly greater levels of lung injury by all of these criteria than did the wild-type mice. We conclude that iNOS knockout mice are more susceptible to acute lung damage induced by exposure to ozone than are wild-type C57B1/6 mice and that protein nitration is associated with the degree of inflammation and not dependent on iNOS-derived nitric oxide.",
keywords = "Inflammation, Macrophage inflammatory protein-2, Matrix metalloproteinase-9, Nitric oxide, Nitrotyrosine",
author = "Nicholas Kenyon and {Van Der Vliet}, Albert and Schock, {Bettina C.} and Tatsuya Okamoto and McGrew, {Gabrielle M.} and Last, {Jerold A}",
year = "2002",
language = "English (US)",
volume = "282",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "3 26-3",

}

TY - JOUR

T1 - Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice

AU - Kenyon, Nicholas

AU - Van Der Vliet, Albert

AU - Schock, Bettina C.

AU - Okamoto, Tatsuya

AU - McGrew, Gabrielle M.

AU - Last, Jerold A

PY - 2002

Y1 - 2002

N2 - Mice deficient in inducible nitric oxide synthase (iNOS; C57B1/6Ai-[KO]NOS2 N5) or wild-type C57B1/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclear leukocytes. The iNOS knockout mice showed significantly greater levels of lung injury by all of these criteria than did the wild-type mice. We conclude that iNOS knockout mice are more susceptible to acute lung damage induced by exposure to ozone than are wild-type C57B1/6 mice and that protein nitration is associated with the degree of inflammation and not dependent on iNOS-derived nitric oxide.

AB - Mice deficient in inducible nitric oxide synthase (iNOS; C57B1/6Ai-[KO]NOS2 N5) or wild-type C57B1/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclear leukocytes. The iNOS knockout mice showed significantly greater levels of lung injury by all of these criteria than did the wild-type mice. We conclude that iNOS knockout mice are more susceptible to acute lung damage induced by exposure to ozone than are wild-type C57B1/6 mice and that protein nitration is associated with the degree of inflammation and not dependent on iNOS-derived nitric oxide.

KW - Inflammation

KW - Macrophage inflammatory protein-2

KW - Matrix metalloproteinase-9

KW - Nitric oxide

KW - Nitrotyrosine

UR - http://www.scopus.com/inward/record.url?scp=0036081341&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036081341&partnerID=8YFLogxK

M3 - Article

C2 - 11839550

AN - SCOPUS:0036081341

VL - 282

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 3 26-3

ER -