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Forming and immunological properties of some lipopolysaccharide-chitosan complexes.

作者信息

Yermak Irina M, Davidova Viktoria N, Gorbach Vladimir I, Luk'yanov Pavel A, Solov'eva Tamara F, Ulmer Arthur J, Buwitt-Beckmann Ute, Rietschel Ernst T, Ovodov Yury S

机构信息

Pacific Institute of Bioorganic Chemistry, Far East Branch of the Russian Academy of Sciences, 159, Pr. 100-letiya, 690022 Vladivostok, Russia.

出版信息

Biochimie. 2006 Jan;88(1):23-30. doi: 10.1016/j.biochi.2005.07.004. Epub 2005 Aug 18.

DOI:10.1016/j.biochi.2005.07.004
PMID:16181724
Abstract

The complex formation of lipopolysaccharide (LPS) with chitosan (Ch) was demonstrated using sedimentation velocity analysis in the analytical ultracentrifuge, centrifugation in glycerol gradient and isopicnic centrifugation in cesium chloride. An addition of Ch to the Escherichia coli and Yersinia pseudotuberculosis LPS solutions was found to result in formation of the stable LPS-Ch complexes. The interaction is a complicated process and depends on time and reaction temperature, as well as on the molecular weight of chitosan. A stable LPS-Ch complex could be formed only after preliminary incubation of the initial components at an elevated temperature (37 degrees C). It should be noted that process of LPS complexation with Ch is accompanied by additional dissociating of LPS. The complex formation was shown to be a result not only of ionic binding, but also of other types of interactions. The interaction of Ch with LPS was shown to modulate significantly the biological activity of LPS. The LPS-Ch complex (1:5 w/w) was shown to possess much lower toxicity in a comparison with the parent LPS at injection to mice in the similar concentration. The LPS-Ch complex was shown to maintain an ability to induce of IL-8 and TNF, but induction of IL-8 and TNF biosynthesis by the LPS-Ch complex was lower than that by the parent LPS. The complex LPS-Ch, similarly to the parent LPS, was found stimulated the formation of the IL-8 in the dose-dependent manner in the human embryonal kidney cells (HEK 293 cells) transfected with TLR4 in combination with MD2.

摘要

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