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Blood, 15 March 2001, Vol. 97, No. 6, pp. 1742-1749
IMMUNOBIOLOGY
Selective inhibition of interleukin-4 gene expression in human T
cells by aspirin
Antonella Cianferoni,
John
T. Schroeder,
Jean Kim,
John W. Schmidt,
Lawrence M. Lichtenstein,
Steve N. Georas, and
Vincenzo Casolaro
From the Departments of Medicine and Otolaryngology,
The Johns Hopkins School of Medicine, Baltimore, MD.
Previous studies indicated that aspirin (acetylsalicylic acid
[ASA]) can have profound immunomodulatory effects by regulating cytokine gene expression in several types of cells. This study is the
first in which concentrations of ASA in the therapeutic range were
found to significantly reduce interleukin (IL)-4 secretion and RNA
expression in freshly isolated and mitogen-primed human CD4+ T cells. In contrast, ASA did not affect IL-13,
interferon- , and IL-2 expression. ASA inhibited IL-4, but not IL-2,
promoter-driven chloramphenicol acetyltransferase expression in
transiently transfected Jurkat T cells. The structurally unrelated
nonsteroidal anti-inflammatory drugs indomethacin and flurbiprofen
did not affect cytokine gene expression in T cells, whereas the weak
cyclo-oxygenase inhibitor salicylic acid was at least as effective as
ASA in inhibiting IL-4 expression and promoter activity. The inhibitory
effect of ASA on IL-4 transcription was not mediated by decreased
nuclear expression of the known salicylate target nuclear factor
(NF)- B and was accompanied by reduced binding of an inducible
factor to an IL-4 promoter region upstream of, but not overlapping, the NF of activated T cells- and NF-B-binding P1 element. It is
concluded that anti-inflammatory salicylates, by means of a previously
unrecognized mechanism of action, can influence the nature of adaptive
immune responses by selectively inhibiting the expression of IL-4, a critical effector of these responses, in CD4+ T cells.
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