Induction of liver-associated transforming growth factor beta 1 (TGF-beta 1) mRNA expression by carbon tetrachloride leads to the inhibition of T helper 2 cell-associated lymphokines

Toxicology and Applied Pharmacology
Y J JeonN E Kaminski

Abstract

Acute treatment of B6C3F1 mice with a hepatotoxic dose (500 mg/kg) of carbon tetrachloride (CCl4) produced a marked but transient increase in transforming growth factor beta 1 (TGF-beta 1) mRNA expression in the liver within 24 hr. We have previously shown that an identical dose of CCl4 also produces a marked increase in serum TGF-beta 1 concentrations which peak at 48 hr and produce a marked inhibition of the anti-sRBC IgM antibody forming cell (AFC) response. Similar increases in TGF-beta 1 transcripts scripts in the liver were also induced by an acute hepatotoxic dose (600 mg/kg) of acetaminophen. No increase in TGF-beta 1 mRNA expression was detected in the spleen following treatment with either agent. Direct addition of TGF-beta 1 (0.05-1.0 ng/ml) to naive splenocyte cultures produced a marked and dose-related inhibition of the anti-sRBC IgM AFC response. Under the same conditions, TGF-beta 1 induced a marked decrease in IL-4 and IL-5 mRNA expression in sRBC-sensitized splenocytes. Concomitantly, TGF-beta 1 induced a rapid increase in NF-kappa B/Rel trans-acting factor binding within the first 24 hr post-sRBC sensitization of splenocytes. Conversely, NF-kappa B/Rel binding activity was inhibited on Days 2 through 4 in sRBC...Continue Reading

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Citations

May 28, 2019·Toxicological Sciences : an Official Journal of the Society of Toxicology·Matthew McMillinSharon DeMorrow

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