β-Glucan derived from Aureobasidium pullulans is effective for the prevention of influenza in mice

PLoS One. 2012;7(7):e41399. doi: 10.1371/journal.pone.0041399. Epub 2012 Jul 23.

Abstract

β-(1→3)-D-glucans with β-(1→6)-glycosidic linked branches produced by mushrooms, yeast and fungi are known to be an immune activation agent, and are used in anti-cancer drugs or health-promoting foods. In this report, we demonstrate that oral administration of Aureobasidium pullulans-cultured fluid (AP-CF) enriched with the β-(1→3),(1→6)-D-glucan exhibits efficacy to protect mice infected with a lethal titer of the A/Puerto Rico/8/34 (PR8; H1N1) strain of influenza virus. The survival rate of the mice significantly increased by AP-CF administration after sublethal infection of PR8 virus. The virus titer in the mouse lung homogenates was significantly decreased by AP-CF administration. No significant difference in the mRNA expression of inflammatory cytokines, and in the population of lymphocytes was observed in the lungs of mice administered with AP-CF. Interestingly, expression level for the mRNA of virus sensors, RIG-I (retinoic acid-inducible gene-I) and MDA5 (melanoma differentiation-associated protein 5) strongly increased at 5 hours after the stimulation of A. pullulans-produced purified β-(1→3),(1→6)-D-glucan (AP-BG) in murine macrophage-derived RAW264.7 cells. Furthermore, the replication of PR8 virus was significantly repressed by pre-treatment of AP-BG. These findings suggest the increased expression of virus sensors is effective for the prevention of influenza by the inhibition of viral replication with the administration of AP-CF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Animals
  • Ascomycota / metabolism*
  • Cell Line
  • Culture Media, Conditioned / metabolism
  • Cytokines / biosynthesis
  • DEAD-box RNA Helicases / metabolism
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / immunology
  • Immunization / methods*
  • Influenza A Virus, H1N1 Subtype / immunology
  • Influenza A Virus, H1N1 Subtype / pathogenicity
  • Intercellular Signaling Peptides and Proteins / biosynthesis
  • Interferon-Induced Helicase, IFIH1
  • Lung / drug effects
  • Lung / immunology
  • Lung / metabolism
  • Lung / virology
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / metabolism
  • Macrophages / virology
  • Male
  • Membrane Proteins / metabolism
  • Mice
  • Nerve Tissue Proteins / metabolism
  • Orthomyxoviridae Infections / prevention & control*
  • Receptors, Cell Surface
  • Survival Rate
  • Time Factors
  • beta-Glucans / metabolism
  • beta-Glucans / pharmacology*

Substances

  • Culture Media, Conditioned
  • Cytokines
  • Intercellular Signaling Peptides and Proteins
  • Membrane Proteins
  • Nerve Tissue Proteins
  • Receptors, Cell Surface
  • Robo3 protein, mouse
  • beta-Glucans
  • Ifih1 protein, mouse
  • DEAD-box RNA Helicases
  • Interferon-Induced Helicase, IFIH1