Opsonic fibronectin deficiency in the etiology of starvation-induced reticuloendothelial phagocytic dysfunction

The role of nutritional deficiencies in mediating host defense failure is increasingly recognized. This study evaluated the effect of starvation on serum opsonic fibronectin levels and reticuloendothelial function in the rat. Over a period of 5 days of starvation serum immunoreactive opsonic fibronectin had fallen to 62% of control levels (458 ± 20 μg/ml). This correlated closely ( r = 0.85, P < 0.05) with a fall in bioassayable opsonic activity. Addition of purified opsonic fibronectin to plasma obtained from starved rats restored its ability to stimulate in vitro Kupffer cell phagocytic activity. Reticuloendothelial phagocytic function in vivo was significantly depressed after 5 days starvation as reflected by prolonged blood retention and decreased hepatic Kupffer cell uptake of a test colloid. Intravenous fibronectin therapy (2 mg/100 g), 1 hr prior to assessment of RE function, significantly ( P < 0.05) improved but did not fully normalize blood clearance and hepatic uptake. These data suggest the RES phagocytic host defense failure in the nutritionally compromised patient may occur, in part, as a consequence of opsonic fibronectin deficiency.