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 language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Lung Cellular and Molecular Physiology |
| Volume | 282 |
| Issue number | 3 26-3 |
| State | Published - 2002 |
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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 journal › Article
}
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
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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 -