Although fibronectin does not act as a direct opsonin as originally described, it does mediate important interactions with phagocytes throughout the inflammatory process. Fragments of fibronectin released by neutrophil proteases are chemoattractants for monocytes. Moreover, subendothelial matrix fibronectin and "inflammatory" fibronectin released from phagocytes enhance phagocyte adherence to host tissues at an inflammatory site. Fibronectin also increases chemokinesis. Once the phagocyte enters tissues, fibronectin promotes C3- and Fc-receptor activation, allowing complement-coated bacteria to be ingested. Finally, fibronectin enhances the bactericidal activity of monocytes. Thus, fibronectin plays an important, but indirect role, in the activities of phagocytes.
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