| Abstract | Endotoxin (lipopolysaccharide [LPS]) released during gram-negative bacterial infection induces varieties of cytokines which directly and/or indirectly cause shock, disseminated intravascular coagulation, and death. We previously showed that lysozyme (LZM) was an LPS-binding protein and inhibited various immunomodulating activities of LPS. In this study, we examined the effect of LZM on the LPS-triggered septic shock model induced by carrageenan treatment and assessed by tumor necrosis factor production. The data presented in this report strongly suggest that LZM-LPS complex formation completely abrogates tumor necrosis factor production and the mortality caused by LPS and that LZM may be useful for the treatment of endotoxin shock. |
| Authors | K Takada, N Ohno, T Yadomae
(Affiliation: Laboratory of Immunopharmacology of Microbial Products, Tokyo College of Pharmacy, Japan.)
|
| Journal | Infection and immunity
(Infect Immun)
Vol. 62
Issue 4
Pg. 1171-5
(Apr 1994)
ISSN: 0019-9567 UNITED STATES |
| PMID | 8132323
(Publication Type: Journal Article)
|
| Chemical References |
- Lipopolysaccharides
- Tumor Necrosis Factor-alpha
- Muramidase
|
| Topics |
- Animals
- Escherichia coli
(pathogenicity)
- Lipopolysaccharides
(metabolism, pharmacology)
- Male
- Mice
- Mice, Inbred ICR
- Muramidase
(metabolism, pharmacology)
- Shock, Septic
(mortality)
- Tumor Necrosis Factor-alpha
(biosynthesis)
|
