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Prostaglandin E₂ Modulation of p59^fyn Tyrosine Kinase in T Lymphocytes During Sepsis¹

Mashkoor A. Choudhry^*, Shahab Uddin and Mohammed M. Sayeed^2,*

^* Departments of Physiology and Surgery, and Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, Maywood, IL 60153; and Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612

Prostaglandin E₂ (PGE₂) has been implicated in the suppression of T cell IL-2 production and proliferation during burn and sepsis. The present study evaluated the potential intracellular mechanism of suppressed T cell responses by assessing the activation of p59^fyn kinase in T cells from septic rats as well as the T cells incubated with PGE₂. p59^fyn is known to regulate T cell functions. Sepsis was induced in rats by implanting fecal pellets containing Escherichia coli (150 CFU) and Bacteroides fragilis (10⁴ CFU) into the abdominal cavity. For the assessment of PGE₂ role in sepsis, a group of septic rats were treated with indomethacin, which inhibits endogenous PGE₂ synthesis. As assessed by immunoblotting or in vitro kinase assay, a more than 40% inhibition of p59^fyn phosphorylation and kinase activity was observed in septic rat T cells compared with the T cells from sterile or control rats. A similar inhibition in p59^fyn phosphorylation and kinase activity was observed in PGE₂-treated T cells compared with the T cells incubated in the absence of PGE₂. The septic-related suppression in p59^fyn phosphorylation and kinase activity in T cells was prevented in rats treated with indomethacin. We observed that the inhibition in p59^fyn activation in septic or PGE₂-treated T cells was due primarily to a suppression in p59^fyn phosphorylation and not due to alterations in p59^fyn protein expression. These findings suggest that PGE₂ released during sepsis could contribute to the sepsis-related suppression in T cell proliferation by attenuating p59^fyn phosphorylation and its kinase activity.

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