Cannabinoids prevent TLR2‐induced inflammation in human glioma cells

The inflammatory network of the central nerve system is orchestrated collaboration of neuronal and non‐neuronal cells, and modulated by diverse molecules. Toll‐liken receptors (TLRs) play critical role of innate immune and inflammatory responses in mammals. Bacterial components recognized by TLR2 an...

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Bibliographic Details
Published in:The FASEB journal Vol. 25; p. 650.20
Main Authors: Echigo, Ryosuke, Sugimoto, Naotoshi, Yachie, Akihiro, Ohono‐Shosaku, Takako
Format: Journal Article
Language:English
Published: Federation of American Societies for Experimental Biology 01-04-2011
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Summary:The inflammatory network of the central nerve system is orchestrated collaboration of neuronal and non‐neuronal cells, and modulated by diverse molecules. Toll‐liken receptors (TLRs) play critical role of innate immune and inflammatory responses in mammals. Bacterial components recognized by TLR2 and TLR4 are mainly present in the bacterial cell membrane. TLR4 recognizes lippopolysaccaride (LPS), which is a potent innate immune stimulator constituting the outer membrane of gram‐negative bacteria, while TLR2 recognizes peptidoglycan (PGN) which is present in cell membrane of gram‐positive bacteria. Recently, cannabinoids have been shown to prevent TLR4‐dependent inflammatory response in vivo and in vitro. However, the effect of cannabinoids on TLR2‐dependent inflammatory response is still unknown. We investigated the role of cannabinoids in prevention of TLR2‐dependent inflammatory response in human glioma cells. In human glioma U87MG cells, PGN induced phosphorylation of the nuclear factor‐kappa B (NF‐κB) transcription factor, indicating that inflammatory response is activated. However, cannabinoid receptors agonist, WIN55,212‐2, inhibited PGN‐induced NF‐κB phosphorylation. Our results suggest that anti‐inflammatory effect of cannabinoids involved in inhibition of TLR2‐dependent inflammatory response in U87MG.
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.25.1_supplement.650.20