Zymosan Depleted

Hot alkali treated zymosan

Zymosan Depleted was obtained by treating zymosan (an insoluble preparation of Saccharomyces cerevisiae cell wall) with hot alkali to remove its Toll-like receptor (TLR)-stimulating properties. Hence, Zymosan Depleted activates the C-type lectin receptor Dectin-1 but not TLR2.

The use of hot alkali or organic solvents to abrogate the TLR2-dependent response of zymosan whilst preserving the Dectin-1 activity has been described previously [1, 2].

References:

1. Gantner BN. et al., 2003. Collaborative induction of inflammatory responses by dectin-1 and Toll- like receptor 2. J Exp Med. 197(9):1107-17.
2. Ikeda Y. et al., 2008. Dissociation of Toll-like receptor 2-mediated innate immune response to Zymosan by organic solvent-treatment without loss of Dectin-1 reactivity. Biol Pharm Bull.31(1):13-8.

Specifications

Specificity: Dectin-1 agonist

Working concentration: 100 µg/ml

CAS number: 58856-93-2

Contents

• 10 mg zymosan depleted
• 10 ml sterile endotoxin-free water

Description

Zymosan depleted was obtained by treating zymosan with hot alkali to remove all its TLR-stimulating properties. Zymosan depleted activates Dectin-1 but not TLR2. Dectin-1, which is expressed on phagocytes, is a specific receptor for β-glucans [1]. β-Glucans are glucose polymers found in the cell walls of fungi, such as zymosan (a cell wall preparation of Saccharomyces cerevisiae) and Candida albicans. Dectin-1 binds and internalizes β-glucans and mediates the production of reactive oxygen species (ROS), activation of NF-κB and subsequent secretion of proinflammatory cytokines. However, it is now clear that its β-glucan moiety triggers NF-κB activation only through Dectin-1 as treatment with hot alkali or organic solvents abrogates the TLR2-dependent response [2,3]. RAW-Blue™ cells express high levels of endogenous Dectin-1 and therefore can be used as a Dectin-1 reporter cell line. Stimulation of RAW-Blue™ cells with zymosan depleted or heat-killed preparations of yeast induces the activation of NF-κB in a Dectin-dependent manner. NF-κB activation can be readily monitored as RAW-Blue™ cells stably express an NF- κB-inducible SEAP reporter gene.

1. Brown GD. et al., 2003. Dectin-1 mediates the biological effects of beta-glucans. J Exp Med. 197( 9): 1119- 24.
2. Gantner BN. et al., 2003. Collaborative induction of inflam- matory responses by dectin-1 and Toll- likereceptor 2. J Exp Med. 197( 9): 1107- 17.
3. ikeda Y. et al., 2008. Dissociation of Toll- like receptor 2-mediated innate immune response to Zymosan by organic solvent-treatment without loss of Dectin-1 reactivity.Biol Pharm Bull.31( 1): 13-8.