| First Author | Kobayashi Y | Year | 2000 |
| Journal | J Pathol | Volume | 192 |
| Issue | 2 | Pages | 263-72 |
| PubMed ID | 11004705 | Mgi Jnum | J:65024 |
| Mgi Id | MGI:1891588 | Doi | 10.1002/1096-9896(2000)9999:9999<::AID-PATH692>3.0.CO;2-U |
| Citation | Kobayashi Y, et al. (2000) Role of macrophage scavenger receptor in endotoxin shock. J Pathol 192(2):263-72 |
| abstractText | Lipopolysaccharide (LPS) is known to bind to several receptors on macrophages, including CD14 and macrophage scavenger receptor class A types I and II (MSR-A), and stimulates macrophages to release various inflammatory mediators. MSR-A recognizes a broad range of polyanionic ligands such as chemically modified lipoproteins, LPS of Gram-negative bacteria, and lipoteichoic acid of Gram-positive bacteria, suggesting a role in host defence. In this study, mice lacking MSR-A were used to elucidate the role of MSR-A in endotoxin shock. Peritoneal macrophages from MSR-A-deficient (MSR-A(-/-)) mice bound less remarkably to LPS than those from wild-type (MSR-A(+/+)) mice and the binding activity of MSR-A(+/+) macrophages to LPS was reduced by the addition of an anti-MSR-A antibody. Clearance of LPS in serum was retarded in MSR-A(-/-) mice after intraperitoneal administration of LPS. LPS-induced expression of cytokines in the liver was similar in MSR-A(+/+) and MSR-A(-/-) mice, but levels of interleukin (IL)-1beta expression and serum IL-1beta were lower in MSR-A(-/-) mice. Administration of large doses of LPS resulted in a higher mortality of MSR-A(+/+) mice and pretreatment with an IL-1 receptor antagonist reduced the mortality. Thus, MSR-A-mediated macrophage activation plays a negative role in protecting mice from endotoxin shock by enhancing IL-1beta production by macrophages. Copyright 2000 John Wiley & Sons, Ltd. |
