Plasmodium berghei malaria: Effects of acute-phase serum and erythrocyte-bound immunoglobulins on erythrophagocytosis by rat peritoneal macrophages

Abstract

Acute-phase serum (APS) collected from Plasmodium berghei-infected rats inhibited phagocytosis of trypsinized rat erythrocytes and of erythrocytes from P. berghei-infected rats. Macrophages (Mφ) incubated with APS or heat-aggregated acute-phase serum (HAAPS) for 6 h, followed by 18 h incubation in serum-free medium, exhibited significantly higher levels of phagocytosis than Mφ similarly cultured but with normal rat serum. When APS was present at the time of assay, it inhibited erythrophagocytosis by Mφ which had been in culture for 0 or 24 h. Mφ activation by HAAPS was inhibited by 2-deoxy-D-glucose, which suggests that activation by HAAPS is Fc-receptor mediated. Adsorption of APS with staphylococcal protein A abrogated the ability of APS to inhibit phagocytosis and that of HAAPS to effect Mφ activation, suggesting that immune complexes are involved in both processes. Surface-bound immunoglobulins eluted from erythrocytes of P. berghei-infected rats promoted phagocytosis of trypsinized erythrocytes by HAAPS-activated Mφ but not by resting Mφ. These results indicate that the immunoglobulins which bind to infected or damaged erythrocytes during malarial infections promote erythrophagocytosis by activated Mφ and that the immune complexes in serum from rats with acute malaria may inhibit erythrophagocytosis early in the infection but may, over time, induce changes in the Mφ which later facilitate erythrophagocytosis.