Immunovascular communication: activation and deactivation of murine endothelial cell nitric oxide synthase by cytokines.

A murine endothelial cell line, send1, was found to produce substantial amounts of nitric oxide, particularly after activation with cytokines. The endothelial cell activation paralleled that of macrophages. Macrophage deactivation opposing activation has recently been brought into focus. We therefore studied the cytokine-mediated deactivation of endothelial cells in send1 and vascular strips. Our observations document that activation of nitric oxide synthase of endothelial cells can be counterbalanced by deactivating cytokines such as interleukin-4, interleukin-8, interleukin-10 and transforming growth factor-beta. Deactivation of nitric oxide synthase in endothelial cells might be an essential mechanism for the control of immune-mediated vasodilatation or septic shock and represents a novel mechanism of communication between the immune and the vascular systems.