| First Author | MacMicking JD | Year | 1995 |
| Journal | Cell | Volume | 81 |
| Issue | 4 | Pages | 641-50 |
| PubMed ID | 7538909 | Mgi Jnum | J:25511 |
| Mgi Id | MGI:73227 | Doi | 10.1016/0092-8674(95)90085-3 |
| Citation | MacMicking JD, et al. (1995) Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase [published erratum appears in Cell 1995 Jun 30;81(7):following 1170]. Cell 81(4):641-50 |
| abstractText | Mice deficient in inducible nitric oxide synthase (iNOS) were generated to test the idea that iNOS defends the host against infectious agents and tumor cells at the risk of contributing to tissue damage and shock. iNOS-/-mice failed to restrain the replication of Listeria monocytogenes in vivo or lymphoma cells in vitro. Bacterial endotoxic lipopolysaccharide (LPS) caused shock and death in anesthetized wild-type mice, but in iNOS-/-mice, the fall in central arterial blood pressure was markedly attenuated and early death averted. However, unanesthetized iNOS-/-mice suffered as much LPS-induced liver damage as wild type, and when primed with Propionobacterium acnes and challenged with LPS, they succumbed at the same rate as wild type. Thus, there exist both iNOS-dependent and iNOS-independent routes to LPS-induced hypotension and death. |
