title: Binding of lysozyme to lipopolysaccharide suppresses tumor necrosis factor production in vivo.
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.affiliation: Laboratory of Immunopharmacology of Microbial Products, Tokyo College of Pharmacy, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Takada
authors.forename: N
authors.initials: N
authors.lastname: Ohno
authors.forename: T
authors.initials: T
authors.lastname: Yadomae
mesh_terms: D000818:Animals; D004926:Escherichia coli / Q000472:pathogenicity; D008070:Lipopolysaccharides / Q000378:metabolism / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009113:Muramidase / Q000378:metabolism / Q000494:pharmacology*; D012772:Shock, Septic / Q000401:mortality; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009113:Muramidase