beta-Glucan attenuates TLR2- and TLR4-mediated cytokine production by microglia.

Abstract:

:Microglia, the resident immune cells of the brain, are activated in response to any kind of CNS injury, and their activation is critical for maintaining homeostasis within the CNS. However, during inflammatory conditions, sustained microglial activation results in damage to surrounding neuronal cells. beta-Glucans are widely recognized immunomodulators, but the molecular mechanisms underlying their immunomodulatory actions have not been fully explored. We previously reported that beta-glucans activate microglia through Dectin-1 without inducing significant amount of cytokines and chemokines. Here, we show that particulate beta-glucans attenuate cytokine production in response to TLR stimulation; this inhibitory activity of beta-glucan is mediated by Dectin-1 and does not require particle internalization. At the molecular level, beta-glucan suppressed TLR-mediated NF-kappaB activation, which may be responsible for the diminished capacity of microglia to produce cytokines in response to TLR stimulation. Overall, these results suggest that beta-glucans may be used to prevent or treat excessive microglial activation during chronic inflammatory conditions.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Shah VB,Williams DL,Keshvara L

doi

10.1016/j.neulet.2009.04.039

subject

Has Abstract

pub_date

2009-07-24 00:00:00

pages

111-5

issue

3

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(09)00523-0

journal_volume

458

pub_type

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