Premium
The Effects of IgG Anti D, IgG Anti D Coated Red Blood Cells and Lysed Red Blood Cells on Macrophage Viability, Morphology and Function
Author(s) -
Ellis April,
Hickman Tyrah,
Hullitt JoAnna,
Tucci Michelle,
Benghuzzi Ham,
Cameron Joseph A.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.628.22
Subject(s) - macrophage , chemistry , lysis , antibody , immunology , phagocytosis , red blood cell , glutathione , microbiology and biotechnology , immunoglobulin g , viability assay , andrology , cell , biology , biochemistry , medicine , in vitro , enzyme
Immunoglobulin G (IgG) deposition at tissue sites leads to macrophage accumulation and organ injury, although the mechanism for injury is not known. The goal of this study was to investigate the interaction of IgG anti D alone, IgG anti D coated red blood cells (RBCs), or lysed RBCs with macrophage cells over time. Cell viability, cellular glutathione membrane damage, morphology, and nitric oxide (NO) were evaluated. Cell numbers were elevated in the lysed red blood cell treatment for the duration of the experiment. Cellular glutathione concentrations were similar to control values for all treated groups compared to the control for the first 48 hours. Cells exposed to IgG anti D coated RBCs showed the lowest glutathione values after 72 hours. Cellular damage was evident for the duration of the study in treated groups compared to control. NO was evident in IgG anti D and IgG anti D coated RBCs for the duration of the study, whereas lysed red blood cells did not increase NO. Overall, the biochemical and cellular staining results possibly indicate that NO is a receptor mediated event and phagocytosis may cause increased malondialdehyde (MDA) levels. Evaluating the interaction of macrophages with IgG may advance our understanding of macrophage involvement in organ injury due to the deposition of IgG. Supported in part by NIGMS‐NIH Grant R25 GM50117.