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Effects of the polysaccharide chain of lipopolysaccharide in an experimental massive hepatic cell necrosis model
Y Mizoguchi1, Y Sakagami, H Kuboi
1Third Department of Internal Medicine, Osaka City University Medical School, Japan.
Abstract:
When small amounts (1 microgram) of lipopolysaccharide (LPS) purified from Salmonella minnesota (SM) wild, SM R60 and SM R345 were intravenously injected into mice 7 days after heat-killed Propionibacterium acnes was intravenously injected, massive hepatic cell necrosis was induced and most of the mice died within 24 hours. However, when LPS from SM R345 treated galactosidase, SM R5 and SM R7 and lipid A from SM R595 were administered, the survival rate was much higher and no histological changes of the liver such as necrosis could be seen in any of the mice. In each of the LPS used in this study, the structure of the polysaccharide chain was different and it was shorter in the following order: SM wild----SM R60----SM R345----SM R345 treated with galactosidase----SM R5----SM R7----SM R595. This suggests that the polysaccharide chain of LPS plays an important role in the induction of massive hepatic cell necrosis in this experimental model.
Insights
Lipopolysaccharide (LPS) from Salmonella minnesota induced liver necrosis and death in mice. Shorter polysaccharide chains on LPS reduced these toxic effects, indicating their crucial role.
Area of Science:
- Immunology
- Toxicology
- Microbiology
Background:
- Lipopolysaccharide (LPS) is a major component of Gram-negative bacteria.
- Heat-killed Propionibacterium acnes can prime the host for exaggerated responses to LPS.
Purpose of the Study:
- To investigate the role of the lipopolysaccharide (LPS) polysaccharide chain length in inducing hepatic cell necrosis.
- To determine the relationship between LPS structure and toxicity in a mouse model.
Main Methods:
- Intravenous injection of varying lengths of Salmonella minnesota LPS into mice pre-treated with heat-killed Propionibacterium acnes.
- Assessment of hepatic cell necrosis and survival rates.
Main Results:
- LPS with longer polysaccharide chains induced massive hepatic cell necrosis and high mortality.
- LPS with shorter polysaccharide chains or lipid A alone resulted in higher survival rates and no observable liver damage.
- A clear inverse correlation was observed between LPS polysaccharide chain length and toxicity.
Conclusions:
- The polysaccharide chain length of LPS is a critical determinant of its ability to induce severe liver toxicity and mortality.
- Modifications in LPS structure, specifically shortening the polysaccharide chain, can significantly attenuate its toxic effects.