Glucan induced modification of experimental Staphylococcus aureus infection in normal, leukemic and immunosuppressed mice.
Glucan, a beta 1 leads to 3 polyglucosidic component of Saccharomyces cerevisiae, was evaluated for its ability to provide nonspecific resistance to S. aureus septicemia in AKR/J mice. Intravenous injection of glucan (0.45 mg/mouse) 7 and 4 days prior to intravenous challenge with S. aureus (1.0 x 10(9)) resulted in a significantly increased survival as compared to control mice. Histological examination of the kidneys revealed that glucan decreased tissue necrosis associated with systemic staphylococcal disease. A post-treatment regimen of glucan significantly enhanced survival of AKR/J mice with lymphocytic leukemia as well as  leukemic mice with experimentally induced systemic staphylococcal infection. The effect of glucan on S. aureus septicemia was also evaluated in cyclophosphamide-treated mice. Glucan increased peripheral leukocyte counts as well as significantly enhanced survival of cyclophosphamide-treated mice with systemic S. aureus infection. Histopathological examination revealed that glucan administration markedly inhibited renal and hepatic pathology in cyclophosphamide-treated mice following intravenous challenge with S. aureus. These data denote that glucan provides nonspecific resistance to bacterial sepsis in normal, leukemic as well as immunosuppressed mice.
D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D005936:Glucans / Q000494:pharmacology*; D007165:Immunosuppression Therapy; D007668:Kidney / Q000473:pathology; D007942:Leukemia, Experimental / Q000150:complications / Q000276:immunology* / Q000401:mortality; D007958:Leukocyte Count; D008099:Liver / Q000473:pathology; D008297:Male; D051379:Mice; D008806:Mice, Inbred AKR; D013203:Staphylococcal Infections / Q000150:complications / Q000276:immunology* / Q000517:prevention & control
D005936:Glucans; D003520:Cyclophosphamide