Data from: Oral administration of Pantoea agglomerans-derived lipopolysaccharide prevents development of atherosclerosis in high-fat diet-fed apoE-deficient mice via ameliorating hyperlipidemia, pro-inflammatory mediators and oxidative responses
Pantoea agglomerans (P. agglomerans) is a Gram-negative bacterium that grows symbiotically with various edible plants, and the oral or sublingual administration of lipopolysaccharide derived from P. agglomerans (LPSp) have been suggested to contribute to prevention of immune-related diseases. Our pr...
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Zusammenfassung: | Pantoea agglomerans (P. agglomerans) is a Gram-negative bacterium that
grows symbiotically with various edible plants, and the oral or sublingual
administration of lipopolysaccharide derived from P. agglomerans (LPSp)
have been suggested to contribute to prevention of immune-related
diseases. Our previous study indicated that orally administered LPSp was
shown to exhibit an LDL-lowering effect in hyperlipidemic volunteers;
however, a preventive effect of LPSp on atherosclerosis is unclear. The
present study attempted to evaluate the anti-atherosclerotic effect by
LPSp in a mouse model of high-fat diet (HFD)-induced atherosclerosis. For
16 weeks, apoE-deficient mice were fed an HFD and received drinking water
containing LPSp (0.3 or 1 mg/kg body weight/day). The results showed that
the orally administered LPSp decreased body weight. A significant
reduction in atherosclerotic plaque deposition was observed even with the
lower dose of LPSp. The biochemical analyses showed that LPSp markedly
improved glucose tolerance and reduced plasma LDL and oxidized LDL levels.
In addition, LPSp significantly reduced the production of pro-inflammatory
mediators including MCP-1 (in the plasma), TNF-α and IL-6 (in the colon),
and decreased the oxidative burst activities in the peripheral blood
sample. Taken together, these results suggest the possibility that oral
administration of LPSp can effectively ameliorate HFD-induced
hyperlipidemia and inflammatory/oxidative responses to prevent
atherosclerosis and related metabolic disorders. |
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DOI: | 10.5061/dryad.1ts48 |