| First Author | Hagiwara SI | Year | 1999 |
| Journal | Am J Pathol | Volume | 154 |
| Issue | 3 | Pages | 705-20 |
| PubMed ID | 10079248 | Mgi Jnum | J:53369 |
| Mgi Id | MGI:1332351 | Doi | 10.1016/S0002-9440(10)65317-5 |
| Citation | Hagiwara SI, et al. (1999) Role of macrophage scavenger receptors in hepatic granuloma formation in mice. Am J Pathol 154(3):705-20 |
| abstractText | In mice homozygous for the gene mutation for type I and type II macrophage scavenger receptors (MSR-A), MSR-A(-/- ), the formation of hepatic granulomas caused by a single intravenous injection of heat-killed Corynebacterium parvum was delayed significantly for 10 days after injection, compared with granuloma formation in wild-type (MSR-A(+/+)) mice. In the early stage of granuloma formation, numbers of macrophages and their precursor cells were significantly reduced in MSR-A(-/-) mice compared with MSR-A(+/+) mice. In contrast to MSR-A(+/+) mice, no expression of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, and interferon-gamma mRNA was observed in. MSR-A(-/-) mice by 3 days after injection. Also in MSR-A(-/-) mice, uptake of C. Parvum by Kupffer cells and monocyte-derived macrophages In the early stage of granuloma formation was lower and elimination of C. Parvum from the liver was slower than in MSR-A(+/+) mice, In the livers of MSR-A(+/+) mice, macrophages and sinusoidal endothelial cells possessed MSR-A, but this was not seen in the livers of MSR-A(-/-) mice. In both MSR-A(-/ -) and MSR-A(+/+) mice, expression of other scavenger receptors was demonstrated. These data suggest that MSR-A deficiency impairs the uptake and elimination of C. Parvum by macrophages and delays hepatic granuloma formation, particularly in the early stage. |
