Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase
Autor: | Myrna E. Trumbauer, Daniel S. Fletcher, Karen Sokol, Qiao-wen Xie, Gary J Hom, Carl Nathan, Karla Stevens, John D. MacMicking, Nicole A. Chartrain, John S. Mudget, Nancy I. Hutchinson, Howard Y. Chen |
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Rok vydání: | 1995 |
Předmět: |
Lipopolysaccharide
Molecular Sequence Data medicine.disease_cause General Biochemistry Genetics and Molecular Biology Microbiology Mice chemistry.chemical_compound Listeria monocytogenes In vivo medicine Animals Base Sequence biology Biochemistry Genetics and Molecular Biology(all) Wild type Bacterial Infections medicine.disease Shock Septic Mice Mutant Strains In vitro Lymphoma Nitric oxide synthase chemistry Shock (circulatory) Immunology biology.protein Amino Acid Oxidoreductases Nitric Oxide Synthase medicine.symptom |
Zdroj: | Cell. 81(4):641-650 |
ISSN: | 0092-8674 |
DOI: | 10.1016/0092-8674(95)90085-3 |
Popis: | Mice deficient in inducible nitric oxide synthase (iNOS) were generated to test the idea that !NOS defends the host against infectious agents and tumor cells at the risk of contributing to tissue damage and shock. iNOS -I- 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 -I- mice, the fall in central arterial blood pressure was markedly attenuated and early death averted. However, unanesthetized iNOS -I- 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. |
Databáze: | OpenAIRE |
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