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.