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12,1412,14-PGJ2 Induces IL-8 Production in Human T Cells by a Mitogen-Activated Protein Kinase Pathway1
Cancer Center, University of Rochester, Rochester, NY 14642
Mast cells, platelets, and some macrophages are abundant sources of
PGD2 and its active metabolite
15-deoxy-
12,14-PGJ2 (15-d-PGJ2).
The lipid mediator 15-d-PGJ2 regulates numerous processes,
including adipogenesis, apoptosis, and inflammation. The
15-d-PGJ2 has been shown to both inhibit as well as induce
the production of inflammatory mediators such as TNF-
, IL-1
, and
cyclooxygenase, mostly occurring via a nuclear receptor called
peroxisome proliferator-activated receptor-
(PPAR-). Data
concerning the effects of 15-d-PGJ2 on human T cells and
immune regulation are sparse. IL-8, a cytokine with both chemotactic
and angiogenic effects, is produced by T lymphocytes following
activation. Whether 15-d-PGJ2 can regulate the production
of IL-8 in T cells in unknown. Interestingly, 15-d-PGJ2
treatment of unstimulated T cells induces cell death. In contrast, in
activated human T lymphocytes, 15-d-PGJ2 does not kill
them, but induces the synthesis of IL-8. In this study, we report that
15-d-PGJ2 induced a significant increase in both IL-8 mRNA
and protein from activated human T lymphocytes. The induction of IL-8
by 15-d-PGJ2 did not occur through the nuclear receptor
PPAR-, as synthetic PPAR- agonists did not mimic the
IL-8-inducing effects of 15-d-PGJ2. The mechanism of IL-8
induction was through a mitogen-activated protein kinase and NF-
B
pathway, as inhibitors of both systems abrogated IL-8 protein
induction. Therefore, 15-d-PGJ2 can act as a potent
proinflammatory mediator in activated T cells by inducing the
production of IL-8. These findings show the complexity with which
15-d-PGJ2 regulates T cells by possessing both pro- and
anti-inflammatory properties depending on the activation state of
the cell. The implications of this research also include that caution
is warranted in assigning a solely anti-inflammatory role for
15-d-PGJ2.
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