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Macrophages and Lymphocytes pp 291–306Cite as

Glucan Induced Modification of Experimental Staphylococcus Aureus Infection in Normal, Leukemic and Immunosuppressed Mice

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 121B))

Abstract

Previous studies in our laboratory have demonstrated that glucan, a βl→ polyglucose component of the cell wall of Saccharomyces cerevisiae, nonspecifically activates lymphoreticular tissue (2,7,25). The intravenous administration of glucan results in a hypertrophy of the major RE organs with an intense activation and proliferation of macrophages (30–32). Glucan administration has been demonstrated to promote tumor regression and enhance survival in rats with an allogeneic Shay chloroleukemia (8) as well as in four syngeneic murine tumor models (10). Preliminary clinical investigations have demonstrated that intralesional administration of glucan results in prompt tumor necrosis with a concomitant monocytic infiltrate (23,24). Furthermore, Israel and Edelstein (19) have also reported that intratumoral administration of glucan resulted in necrosis of the lesion with a concomitant resolution of a distant nodule. Topical application of glucan resulted in disappearance of ulcerated lesions (19,23).

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Authors and Affiliations

  1. Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana, USA

    D. L. Williams & N. R. di Luzio

Authors
  1. D. L. Williams
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  2. N. R. di Luzio
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Editor information

Editors and Affiliations

  1. Medical College of Virginia, Richmond, Virginia, USA

    Mario R. Escobar

  2. University of South Florida, Tampa, Florida, USA

    Herman Friedman

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© 1980 Plenum Press, New York

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Williams, D.L., di Luzio, N.R. (1980). Glucan Induced Modification of Experimental Staphylococcus Aureus Infection in Normal, Leukemic and Immunosuppressed Mice. In: Escobar, M.R., Friedman, H. (eds) Macrophages and Lymphocytes. Advances in Experimental Medicine and Biology, vol 121B. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3593-1_25

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  • DOI: https://doi.org/10.1007/978-1-4684-3593-1_25

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-3595-5

  • Online ISBN: 978-1-4684-3593-1

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