| First Author | Rohan PJ | Year | 1997 |
| Journal | Proc Soc Exp Biol Med | Volume | 215 |
| Issue | 3 | Pages | 269-74 |
| PubMed ID | 9207863 | Mgi Jnum | J:41586 |
| Mgi Id | MGI:894073 | Doi | 10.3181/00379727-215-44138 |
| Citation | Rohan PJ, et al. (1997) Macrophage function in mice with a mutation at the microphthalmia (mi) locus. Proc Soc Exp Biol Med 215(3):269-74 |
| abstractText | Microphthalmic (mi/mi) mice are unpigmented, osteopetrotic, mast cell deficient, and exhibit diminished gastric acid secretion and natural killer cell activity, In order to assess the effect of this mutation on macrophage function, we studied superoxide (O-2(-)) and nitric oxide (NO) production, superoxide dismutase (SOD) activity, phagocytic capacity, and tumor cell killing by peritoneal macrophages from mi/mi mice and normal (+/+) litter mates, Macrophages from mi/mi mice, upon activation with phorbol myristate acetate (PMA), generated significantly higher amounts of O-2(-) than did macrophages from their +/+ litter mates, The phagocyte respiratory burst as assessed by nitroblue tetrazolium (NET) reduction assay also displayed a 2-fold enhancement in mi/mi macrophages, The assay of SOD activity revealed significantly lower levels in mi/mi macrophages than in the wild type, Furthermore, in comparison with controls, macrophages from mi/mi mice demonstrated significantly higher levels of NO production and increased capacity to lyse tumor cells upon activation with lipopolysaccharide (LPS) or gamma-interferon (IFN-gamma), The mi mutation, therefore, is associated with reduced macrophage SOD activity, increased O-2(-) and NO production, and enhanced capacity for tumor cell killing, The molecular mechanisms for these changes have not been identified. |
