Lymphokines and platelets promote human monocyte adherence to fibrinogen and fibronectin in vitro.

Monocytes must accumulate in areas of tissue injury and inflammation to effect phagocytosis, antigen presentation, and monokine production. Fibrinogen/fibronectin matrices have been demonstrated in healing wounds and in delayed-type hypersensitivity skin reactions. We have developed an in vitro system for investigation of the ability of fibrinogen and fibronectin matrices to serve as substrata for human peripheral blood monocyte adherence. Monocyte adherence was greatest on matrices of both fibrinogen and fibronectin, less to fibrinogen alone, and least to fibronectin alone. Lymphokines increased adherence of monocytes to all three surfaces but not to albumin-coated surfaces. Addition of platelets also caused a dose-dependent increase in monocyte adherence to all three surfaces. This increased adherence was not a simple function of arachidonic acid metabolites, stable platelet products, nor monocyte binding sites on the platelet membrane. The effect of platelets was not additive to the effect of lymphokines. We conclude that fibrinogen and fibronectin provide a framework for monocyte adherence and that factors present in areas of inflammation and wound healing, such as lymphokines and platelets, can augment this adherence. Such adherence facilitates the transformation of monocytes into macrophages in vitro and may also foster such transformation in vivo.