Abstract
β-Glucans are known for their ability to trigger both protective and damaging immune responses. Here we have explored the role of the beta-glucan receptor Dectin-1 in archetypical models of protective and non-protective immunomodulation induced by beta-glucan rich ligands. In the first model, we explored the role of Dectin-1 in the ability of soluble purified β-glucans to mediate protection against systemic Staphylococcus aureus infection in mice. In the second model, we explored the role of Dectin-1 in zymosan induced multiple organ dysfunction syndrome. In both cases, these β-glucan rich compounds had marked effects in vivo which were unaltered by Dectin-1 deficiency, suggesting that this receptor has a redundant role in these murine models.
Highlights
Introduction bGlucans are glucose polymers that are found in fungal cell walls, plants and some bacteria [1]. b-Glucans are known for their ability to activate leukocytes, and have been of considerable interest as immune modulators, promoting antitumorigenic and anti-microbial activities [2]
We explored the role of Dectin-1 in the ability of soluble purified b-glucans to mediate protection against systemic Staphylococcus aureus infection in mice
We have investigated the involvement of Dectin-1 in both protective and non-protective models of immunomodulation induced by b-glucan rich ligands
Summary
Introduction bGlucans are glucose polymers that are found in fungal cell walls, plants and some bacteria [1]. b-Glucans are known for their ability to activate leukocytes, and have been of considerable interest as immune modulators, promoting antitumorigenic and anti-microbial activities [2]. We explored the role of Dectin-1 in the ability of soluble purified b-glucans to mediate protection against systemic Staphylococcus aureus infection in mice. To explore the role of Dectin-1, a major leukocyte receptor for these carbohydrates, we established a systemic model of infection with S. aureus which resulted in rapid weight loss and more than 50% mortality in untreated mice (Fig. 1A, B).
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