Abstract
Evidence has accumulated over the past several years demonstrating that lung injury following inhalation of irritants like ozone is due, not only to direct effects of the chemical, but also indirectly to the actions of inflammatory mediators released by infiltrating macrophages. Among the mediators involved in the cytotoxic process, reactive nitrogen species (RNS) are of particular interest because of their well-documented cytotoxic potential. Findings that macrophage suppression blocks RNS production and ozone-induced toxicity provide strong support for a role of these cells and inflammatory mediators in lung injury. Recent investigations have focused on understanding pathways by which macrophages become activated to release RNS. One protein that has attracted considerable attention is caveolin-1, a membrane scaffolding molecule that functions to negatively regulate cell signaling. The fact that expression of caveolin-1 is down-regulated in macrophages after ozone inhalation suggests a mechanism controlling the release of cytotoxic mediators by these inflammatory cells.
| Original language | English |
|---|---|
| Title of host publication | Oxidative/Nitrosative Stress and Disease |
| Pages | 60-65 |
| Number of pages | 6 |
| Volume | 1203 |
| DOIs | |
| Publication status | Published - Aug 2010 |
| Externally published | Yes |
Publication series
| Name | Annals of the New York Academy of Sciences |
|---|---|
| Volume | 1203 |
| ISSN (Print) | 00778923 |
| ISSN (Electronic) | 17496632 |
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Keywords
- caveolin
- macrophages
- nitric oxide
- ozone
- TNFα
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Macrophages, reactive nitrogen species, and lung injury. / Laskin, Debra L.; Sunil, Vasanthi R.; Fakhrzadeh, Ladan; Groves, Angela; Gow, Andrew J.; Laskin, Jeffrey D.
Oxidative/Nitrosative Stress and Disease. Vol. 1203 2010. p. 60-65 (Annals of the New York Academy of Sciences; Vol. 1203).Research output: Chapter in Book/Report/Conference proceeding › Conference contribution
}
TY - GEN
T1 - Macrophages, reactive nitrogen species, and lung injury
AU - Laskin, Debra L.
AU - Sunil, Vasanthi R.
AU - Fakhrzadeh, Ladan
AU - Groves, Angela
AU - Gow, Andrew J.
AU - Laskin, Jeffrey D.
PY - 2010/8
Y1 - 2010/8
N2 - Evidence has accumulated over the past several years demonstrating that lung injury following inhalation of irritants like ozone is due, not only to direct effects of the chemical, but also indirectly to the actions of inflammatory mediators released by infiltrating macrophages. Among the mediators involved in the cytotoxic process, reactive nitrogen species (RNS) are of particular interest because of their well-documented cytotoxic potential. Findings that macrophage suppression blocks RNS production and ozone-induced toxicity provide strong support for a role of these cells and inflammatory mediators in lung injury. Recent investigations have focused on understanding pathways by which macrophages become activated to release RNS. One protein that has attracted considerable attention is caveolin-1, a membrane scaffolding molecule that functions to negatively regulate cell signaling. The fact that expression of caveolin-1 is down-regulated in macrophages after ozone inhalation suggests a mechanism controlling the release of cytotoxic mediators by these inflammatory cells.
AB - Evidence has accumulated over the past several years demonstrating that lung injury following inhalation of irritants like ozone is due, not only to direct effects of the chemical, but also indirectly to the actions of inflammatory mediators released by infiltrating macrophages. Among the mediators involved in the cytotoxic process, reactive nitrogen species (RNS) are of particular interest because of their well-documented cytotoxic potential. Findings that macrophage suppression blocks RNS production and ozone-induced toxicity provide strong support for a role of these cells and inflammatory mediators in lung injury. Recent investigations have focused on understanding pathways by which macrophages become activated to release RNS. One protein that has attracted considerable attention is caveolin-1, a membrane scaffolding molecule that functions to negatively regulate cell signaling. The fact that expression of caveolin-1 is down-regulated in macrophages after ozone inhalation suggests a mechanism controlling the release of cytotoxic mediators by these inflammatory cells.
KW - caveolin
KW - macrophages
KW - nitric oxide
KW - ozone
KW - TNFα
UR - http://www.scopus.com/inward/record.url?scp=77956236274&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77956236274&partnerID=8YFLogxK
U2 - 10.1111/j.1749-6632.2010.05607.x
DO - 10.1111/j.1749-6632.2010.05607.x
M3 - Conference contribution
C2 - 20716284
AN - SCOPUS:77956236274
SN - 9781573317849
VL - 1203
T3 - Annals of the New York Academy of Sciences
SP - 60
EP - 65
BT - Oxidative/Nitrosative Stress and Disease
ER -