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- W2003163790 abstract "Microglial activation is an important pathological component in brains of patients with Alzheimer's disease (AD) and fibrillar amyloid β (Aβ) peptides play an important role in microglial activation in AD. However, the mechanisms by which Aβ peptides induce the activation of microglia are poorly understood. The present study underlines the importance of toll-like receptor 2 (TLR2) in mediating Aβ peptide-induced activation of microglia. BV-2 microglial cells and primary microglia isolated from 7 – 9 d old wild type and TLR2 (-/-) mouse pups were stimulated with fibrillar Aβ1–42 peptides followed by analysis of different proinflammatory molecules and surface markers in microglia. Antisense oligonucleotides and functional blocking antibodies were used to block the function of various TLRs on microglia. Furthermore, to examine the hypothesis in vivo, fibrillar Aβ1–42 peptides were microinjected into the cortex of wild type and TLR2 (-/-) mice. Fibrillar Aβ1–42 peptides induced the expression of inducible nitric oxide synthase (iNOS), pro-inflammatory cytokines (TNF–α, IL-1β and IL-6) and integrin markers (CD11b, CD11c and CD68) in mouse primary microglia and BV-2 microglial cells. However, either antisense knockdown of TLR2 or functional blocking antibodies against TLR2 suppressed Aβ1–42-induced expression of pro-inflammatory molecules and integrin markers in microglia. Aβ1–42 peptides were also unable to induce the expression of pro-inflammatory molecules and increase the expression of CD11b in microglia isolated from TLR2 (-/-) mice. Finally, the inability of Aβ1–42 peptides to induce the expression of iNOS and to stimulate the expression of CD11b in vivo in the cortex of TLR2 (-/-) mice highlights the importance of TLR2 in Aβ-induced microglial activation. In addition, ligation of TLR2 alone was also sufficient to induce microglial activation. Consistent to the importance of Myd88 in mediating the function of various TLRs, antisense knockdown of Myd88 also inhibited Aβ1–42 peptide-induced expression of pro-inflammatory molecules. These studies delineate a novel role of TLR2 signaling pathway in mediating fibrillar Aβ peptide-induced activation of microglia and suggest that antagonists of TLR2 may have therapeutic importance in AD. Supported by grants from Alzheimer's Association (IIRG-07–58684) and NIH (NS39940 and NS48923)." @default.
- W2003163790 created "2016-06-24" @default.
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- W2003163790 date "2008-07-01" @default.
- W2003163790 modified "2023-09-25" @default.
- W2003163790 title "P3-361: Microglial activation by fibrillar amyloid-beta peptides requires toll-like receptor 2" @default.
- W2003163790 doi "https://doi.org/10.1016/j.jalz.2008.05.1931" @default.
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