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β‐1,3‐Glucan given orally modulates immunomyelopoietic activity and enhances the resistance of tumour‐bearing mice
Author(s) -
Torello CO,
SouzaQueiroz J,
Queiroz MLS
Publication year - 2012
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2011.05655.x
Subject(s) - bone marrow , immune system , myeloid , progenitor cell , stromal cell , cytokine , interferon , medicine , immunology , endocrinology , innate immune system , pharmacology , biology , stem cell , microbiology and biotechnology
Summary β‐Glucans have been reported to be potent adjuvants in stimulating innate and adaptive immune responses. The aim of the present study was to determine the immunohematopoietic effects of I munoglucan ( HEBRON ) following its oral administration to normal and E hrlich ascites tumour ( EAT )‐bearing mice. Mice were treated with 250, 500 and 1000 mg/kg per day, p.o., I munoglucan (β‐1,3‐glucan extracted from Saccharomyces cerevisae ) for 18 consecutive days. Treatment started 10 days prior to and ended 8 days after tumour inoculation. At 500 and 1000 mg/kg per day, I munoglucan enhanced the life span of EAT ‐bearing mice and prevented myelosuppression and splenomegaly caused by the tumour by increasing the number of granulocyte–macrophage progenitors in the bone marrow and increasing colony‐stimulating activity in the serum. At 500 mg/kg, I munoglucan restored the reduced ability of stromal cells to display myeloid progenitors in long‐term bone marrow cultures of EAT ‐bearing mice and upregulated the production of interleukin ( IL )‐6 and IL ‐1α by these cells, consistent with a higher number of non‐adherent cells. Moreover, 500 mg/kg I munoglucan restored natural killer cell activity in tumour‐bearing mice, consistent with the increased production of interferon ( IFN )‐γ observed. The results of the present study suggest that I munoglucan given orally indirectly modulates immune activity and probably disengages tumour‐induced suppression by producing a higher reserve of myeloid progenitors in the bone marrow in consequence of biologically active cytokine release (colony‐stimulating factors, IL ‐1α, IL ‐6 and IFN ‐γ).