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Ozone induction of cytokine‐induced neutrophil chemoattractant (CINC) and nuclear factor‐κb in rat lung: inhibition by corticosteroids
Author(s) -
Haddad E.-B.,
Salmon M.,
Koto H.,
Barnes P.J.,
Adcock I.,
Chung K.F.
Publication year - 1996
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)01524-8
Subject(s) - chemokine , inflammation , dexamethasone , cytokine , basal (medicine) , lung , nf κb , nfkb1 , chemistry , medicine , ozone , transcription factor , messenger rna , endocrinology , chemotaxis , immunology , biology , biochemistry , receptor , gene , organic chemistry , insulin
We determined in rat lung whether ozone exposure was associated with the expression of the chemokine, cytokine‐induced neutrophil chemoattractant (CINC), and of the transcription factor, NF‐κB. CINC mRNA expression peaked at 2 h after cessation of ozone exposure, and returned to basal levels by 24 h. DNA‐binding activity of NF‐κB showed a marked increase after ozone, maximal at 2 h. Dexamethasone inhibited CINC mRNA and NF‐κB expression, together with neutrophilic inflammation. Our data supports the concept that ozone leads to NF‐κB activation which increases CINC mRNA expression. These series of events could lead to neutrophilic inflammation.