PGE2 suppresses mitogen-induced Ca2+ mobilization in T cells.

PGE2-mediated suppression of T cell proliferation during sepsis could result from altered Ca2+ signaling. The present study evaluated the effects of PGE2 on Ca2+ release from intracellular stores and its influx through the plasma membrane in splenic T cells from Sprague-Dawley rats. Intracellular Ca2+ concentration ([Ca2+]i) responses in individual T cells were assessed using the Ca2+ imaging technique, and the release of Ca2+ from intracellular stores and Ca2+ influx were spectrofluorometrically quantified in T cell suspensions. Under unstimulated conditions, nearly 85% of T cells exhibited [Ca2+]i≤50 nM. After stimulation with concanavalin A (Con A), an increase in [Ca2+]iwas recorded in ∼60% of the cells. The pretreatment of T cells with PGE2 had no apparent effect on [Ca2+]iin resting cells; it significantly suppressed the Con A-induced increase in [Ca2+]iin all of the Con A-responsive cells. Ca2+ release from the intracellular stores contributed to the early spike in [Ca2+]i, and the late phase of elevation in [Ca2+]iwas dependent on Ca2+ influx through the plasma membrane. Our data suggest that PGE2 causes an overall suppression of the Con A-induced [Ca2+]ielevation in T cells via inhibiting both Ca2+ influx and its release from the intracellular stores.