
Priming effect of dextran sulphates on lipopolysaccharide‐induced tumour necrosis factor production in mice
Author(s) -
Kamochi Masayuki,
Ogata Masanori,
Yoshida Shinichi,
Mizuguchi Yasuo,
Shigematsu Akio
Publication year - 1992
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1992.tb04984.x
Subject(s) - lipopolysaccharide , dextran , priming (agriculture) , tumor necrosis factor alpha , chemistry , necrosis , tumor necrosis factor α , microbiology and biotechnology , immunology , medicine , biology , biochemistry , botany , germination
Dextran sulphate (DS) 500 (M.W. 500 000) is commonly used as a reticuloendothelial (RE) blocker. We found that lipopolysaccharide (LPS)‐induced tumour necrosis factor (TNF) production in sera was enhanced when mice were pretreated with DS500. When mice were pretreated with DS1000 (M.W. 1 000 000), TNF activity in sera was also significantly enhanced by the LPS injection in comparison with the saline‐treated group, but not by the pretreatment with the low molecular weight of DS5 (M.W. 5 000), neutral dextran (Dex) 500, or positively‐charged diethylaminoethyl dextran (DEAE‐Dex) 500. The enhancement of LPS‐induced TNF production occurred from 2 h after DS500 pretreatment. Pretreatment with DS500 or DS1000 significantly suppressed the carbon clearance from the blood in mice from 2 h after DS injection, but this suppression was not detected by the pretreatment with DS5, Dex500, or DEAE‐Dex500. We suggest that negative‐charge and high molecular weight are essential for dextran derivatives to enhance LPS‐induced TNF production, and that the enhancing effect of DS is closely related to the suppression of the RE function.