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Differential regulation of oxidative burst by distinct Beta-glucan-binding receptors and signaling pathways in human peripheral blood mononuclear cells

Glycobiology (2014) doi: 10.1093/glycob/cwu005
First published online: January 16, 2014

Nandita Bose1, Lindsay R. Wurst1, Anissa S.H. Chan1, Christine M. Dudney1, Megan L. LeRoux1, Michael E. Danielson1, Paul M. Will1, Sonja E. Nodland1, Myra L. Patchen1, Jurandir J. Dalle Lucca2, Frank J. Lebeda3 and John P. Vasilakos1

  1. Biothera, Eagan, MN 55121 USA
  2. US Army Institute of Surgical Research, Ft. Sam Houston, 78234 USA TX
  3. US Army Medical Research and Materiel Command, Ft. Detrick, MD 21701 USA

Abstract

β-glucans possess broad immunomodulatory properties, including activation of innate immune functions such as oxidative burst activity. The differential roles of complement receptor type 3 and Dectin-1, the known β-glucan receptors and their associated signaling pathways in the generation of oxidative burst induced by different physical forms of Saccharomyces cerevisiae-derived β-glucan were examined in human peripheral blood mononuclear cells. In this study whole glucan particle or immobilized soluble β-glucan was used to represent the phagocytizable or the non-phagocytizable form of a fungus, respectively. Oxidative burst as measured by the formation of superoxide was detected in peripheral blood mononuclear cells in response to whole glucan particle and immobilized soluble β-glucan. Superoxide induction with whole glucan particle was concluded to be Dectin-1-mediated, and required Src family kinases, phosphatidylinositol-3 kinase and protein kinase B/Akt. In contrast, the superoxide induction generated by immobilized soluble β-glucan was complement receptor type 3-mediated and required focal adhesion kinase, spleen tyrosine kinase, phosphatidylinositol-3 kinase, Akt, p38 mitogen activated protein kinase, phospholipase C and protein kinase C. The study results support the hypothesis that human peripheral blood mononuclear cells, specifically monocytes, utilize distinct receptors and overlapping, but distinct, signaling pathways for the oxidative burst in response to challenge by different physical forms of β-glucan.

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Published at wellmune.com on 13 February 2014

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