Activation of the IL-1 gene in UV-irradiated mouse skin: association with inflammatory sequelae and pharmacologic intervention.
The relationship between ultraviolet irradiation, interleukin-1 production, and inflammatory sequelae and the pharmacologic inhibition of these events was investigated in Balb/c mice exposed to ultraviolet irradiation from a bank of six Westinghouse FS40 sunlamps. The resulting edema (66% increase), inflammatory cell infiltration, and rise in the acute-phase reactant (fourfold) serum amyloid P component was preceded by the activation of the interleukin-1 beta gene and enhanced product formation. Administration of dexamethasone, which is known to inhibit interleukin-1 production, inhibited the inflammatory response to ultraviolet irradiation. Thus, production of interleukin-1 may be one of the initial events leading to the consequences of ultraviolet irradiation exposure.
Griswold
D E
DE
Division of Pharmacological Sciences, SmithKline Beecham Pharmaceuticals, Research and Development, King of Prussia, Pennsylvania 19406.
Connor
J R
JR
Dalton
B J
BJ
Lee
J C
JC
Simon
P
P
Hillegass
L
L
Sieg
D J
DJ
Hanna
N
N
D000818:Animals; D015152:Blotting, Northern; D003872:Dermatitis / Q000209:etiology; D003907:Dexamethasone / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000528:radiation effects; D007375:Interleukin-1 / Q000235:genetics* / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009195:Peroxidase / Q000032:analysis; D000683:Serum Amyloid P-Component / Q000032:analysis; D012867:Skin / Q000528:radiation effects*; D014466:Ultraviolet Rays
D007375:Interleukin-1; D000683:Serum Amyloid P-Component; D003907:Dexamethasone; D009195:Peroxidase