Alloimmune B-lymphocytes modify the myocardium contractility-inducing release of SRS-A.

It has been previously demonstrated that murine alloimmune lymphoid cells were able to exert positive or negative inotropic effects on isolated mouse atria depending on the cellular type used. Here we show that BALB/c anti-C3H B-cells induced positive inotropic action on C3H mouse atria. Supernatants of alloimmunized B-cells co-cultivated with C3H myocardium exerted the same biological effect as alloimmune B-cells, indicating that a soluble factor is involved. Inhibitors of lipoxygenase(s) of arachidonic acid metabolism and a SRS-A blocker inhibited the positive effect of immune cells or its supernatants. The effect was prevented when we inhibited the atria lipoxygenase activity. On the other hand, when the inhibitors were applied to effector cells the response was not modified. In addition, supernatants of B-cells cultured with alloextracts were inactive. Supernatants from alloimmune B-cells plus myocardium release higher amounts of LTC4 than those from normal B-cells. It is proposed that SRS-A synthesis is induced in the atria by direct contact with alloimmune B-cells upon recognition of alloantigens expressed by atria cells; which in turn, triggers the positive inotropic effect.