TY - JOUR
T1 - A lectin-like receptor on murine macrophage is involved in the recognition and phagocytosis of human red cells oxidized by phenylhydrazine
AU - Horn, Sara
AU - Gopas, Jacob
AU - Bashan, Nava
PY - 1990/2/15
Y1 - 1990/2/15
N2 - Phenylhydrazine (Phz) is a powerful hemolytic agent which has several effects on both normal and G6PD déficient red blood cells (RBCs). We have studied the mechanism of removal of Phz-damaged human RBCs by murine macrophages. Phagocytosis of Phz-treated RBCs was found to be 50 RBCs/100 mac as compared to 2 RBCs/100 mac of the controls. EGTA and sodium azide inhibited the phagocytosis, indicating a requirement for both calcium ions and energy. Incubation of macrophages with sugars such as d-galactose or d-mannose reduced phagocytosis of Phz-treated RBCs by up to 60%, indicating the involvement of a macrophage lectin-like receptor in the recognition of Phz-treated RBCs. The presence of serum in the phagocytosis assay did not affect either phagocytosis of Phz-treated RBCs or inhibition by sugars. β-Galactosidase, but not neuraminidase, treatment of RBCs caused a significant inhibition in phagocytosis of Phz-treated RBCs. These results suggest that galactosyl residues are exposed on RBC membrane during oxidation, probably not as a result of desialization. We conclude that Phz-treated RBCs are detected as damaged cells mainly due to sugar changes on their membrane, which are directly recognized by lectin-like receptors on the macrophages.
AB - Phenylhydrazine (Phz) is a powerful hemolytic agent which has several effects on both normal and G6PD déficient red blood cells (RBCs). We have studied the mechanism of removal of Phz-damaged human RBCs by murine macrophages. Phagocytosis of Phz-treated RBCs was found to be 50 RBCs/100 mac as compared to 2 RBCs/100 mac of the controls. EGTA and sodium azide inhibited the phagocytosis, indicating a requirement for both calcium ions and energy. Incubation of macrophages with sugars such as d-galactose or d-mannose reduced phagocytosis of Phz-treated RBCs by up to 60%, indicating the involvement of a macrophage lectin-like receptor in the recognition of Phz-treated RBCs. The presence of serum in the phagocytosis assay did not affect either phagocytosis of Phz-treated RBCs or inhibition by sugars. β-Galactosidase, but not neuraminidase, treatment of RBCs caused a significant inhibition in phagocytosis of Phz-treated RBCs. These results suggest that galactosyl residues are exposed on RBC membrane during oxidation, probably not as a result of desialization. We conclude that Phz-treated RBCs are detected as damaged cells mainly due to sugar changes on their membrane, which are directly recognized by lectin-like receptors on the macrophages.
UR - http://www.scopus.com/inward/record.url?scp=0025014762&partnerID=8YFLogxK
U2 - 10.1016/0006-2952(90)90158-H
DO - 10.1016/0006-2952(90)90158-H
M3 - Article
AN - SCOPUS:0025014762
SN - 0006-2952
VL - 39
SP - 775
EP - 780
JO - Biochemical Pharmacology
JF - Biochemical Pharmacology
IS - 4
ER -