The role of plasma fibronectin as a nonantibody, noncomplement opsonin for Staphylococcus aureus

The possible role of plasma fibronectin as a nonantibody, noncomplement opsonin for S. aureus was studied using peripheral blood leukocytes from healthy rabbits. Fibronectin depletion of normal rabbit serum by affinity absorption chromatography reduced the opsonic ability of that serum (p less than 0.05) and resulted in impaired bacterial killing of S. aureus in vitro. The addition of purified fibronectin to fibronectin-depleted serum significantly reversed the opsonic defect (p less than 0.01). The combination of complement inactivation, plus fibronectin depletion, resulted in a severe opsonic deficiency that was much worse than either deficiency alone (p less than 0.05). However, fibronectin alone in the absence of other serum factors was a poor opsonin for S. aureus, suggesting that its major role as an opsonin might be to augment or amplify other serum factors.