Effect of SPG/indomethacin treatment on sepsis, interleukin-6 production, and expression of hepatic cytochrome P450 isoforms in differing strains of mice.

We previously reported that a combination of beta-glucan and indomethacin (IND), a non-steroidal anti-inflammatory drug, was lethal to mice. This lethality was strongly related to translocation of enterobacterial flora to various organs and the development of a systemic inflammation. In this study, we examined expression of microsomal cytochrome P450 (CYP), a drug-metabolizing enzyme mostly found in the liver.

SPG/IND-induced septic shock in a LPS-low responder strain, C3H/HeJ mice.

The administration of beta-glucan (sonifilan; SPG) in combination with a non-steroidal anti-inflammatory drug, indomethacin (IND), induced lethal septic shock in mice. To demonstrate the influence of bacterial lipopolysaccharide (LPS) in this lethal toxicity, LPS non-responder C3H/HeJ mice were used to compare features of sepsis and physicochemical parameters in the present study. The administration of SPG and IND induced the death of C3H/HeJ mice, lowering rectal temperature, reducing body weight, increasing serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels, shortening the gastrointestinal tract, and increasing the GOT/GPT level.

Lincomycin protects mice from septic shock in beta-glucan-indomethacin model.

We have developed a septic shock model in mice by sequential administration of beta-glucan, a biological response modifier, and indomethacin (IND), a nonsteroidal anti-inflammatory drug. Lethality was significantly related to the translocation of gut flora to various organs and mal-adjustment of the cytokine network. In the present study, we have examined the effect of antibiotics on this model to further clarify meanings of microbial flora.

Antibiotics protect against septic shock in mice administered beta-glucan and indomethacin.

We have developed an animal model of sepsis in mice by repeatedly administering beta-glucan, a biological response modifier, and indomethacin (IND), a nonsteroidal anti-inflammatory drug. The combination of these drugs induced bacteremia by translocation of the enterobacterial flora, resulting in increasing the number of activated leukocytes, and inducing hyper cytokinemia. In the present study, we examined the effect of antibiotics on beta-glucan and IND-induced septic shock.

Effect of nitric oxide on beta-glucan/indomethacin-induced septic shock.

We have previously shown that repeated administration of nonsteroidal anti-inflammatory drugs (NSAIDs) to mice treated with beta-glucan, a biological response modifier, induced severe lethality. The lethality would be strongly related to the translocation of enterobacterial flora to the peritoneal cavity and disruption of the cytokine network. Reports suggest that nitric oxide (NO) can have an effective or detrimental role in septic shock.

Enhanced cytokine synthesis of leukocytes by a beta-glucan preparation, SCG, extracted from a medicinal mushroom, Sparassis crispa.

Sparassis crispa is edible mushroom recently cultivable in Japan. It contains significantly high content (approximately 40%) of 6-branched 1,3-beta-D-glucan showing antitumor activity in mice. We recently purified a beta-glucan preparation designated as "SCG.