http://www.cnr.it/ontology/cnr/individuo/prodotto/ID196900
Lipopolysaccharide downregulates fatty acid amide hydrolase expression and increases anandamide levels in human peripheral lymphocytes (Articolo in rivista)
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- Label
- Lipopolysaccharide downregulates fatty acid amide hydrolase expression and increases anandamide levels in human peripheral lymphocytes (Articolo in rivista) (literal)
- Anno
- 2001-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1006/abbi.2001.2500 (literal)
- Alternative label
Maccarrone M, De Petrocellis L, Bari M, Fezza F, Salvati S, Di Marzo V, Finazzi-Agrò A. (2001)
Lipopolysaccharide downregulates fatty acid amide hydrolase expression and increases anandamide levels in human peripheral lymphocytes
in Archives of biochemistry and biophysics (Print); Academic Press, San Diego (Stati Uniti d'America)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Maccarrone M, De Petrocellis L, Bari M, Fezza F, Salvati S, Di Marzo V, Finazzi-Agrò A. (literal)
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- 1. Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, I-00133 Rome, Italy
2. CNR, Ist Chim Mol Interesse Biol, Endocannabinoid Res Grp, I-80072 Arco Felice Napoli, Italy
3. CNR, Ist Cibernetica, I-80072 Arco Felice Napoli, Italy (literal)
- Titolo
- Lipopolysaccharide downregulates fatty acid amide hydrolase expression and increases anandamide levels in human peripheral lymphocytes (literal)
- Abstract
- Lipopolysaccharide (LPS) increases the levels of the endogenous cannabinoid anandamide (N-arachidonoylethanolamine, AFA) in rat macrophages, but the mechanism responsible for this effect has not been elucidated. Here we demonstrate that LPS enhances the levels of AEA (fourfold over controls) also in human lymphocytes. We show that in these cells LPS inhibits the activity of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH), by downregulating the gene expression at transcriptional level. Lymphocytes have also a specific ARA transporter and a functional CB1 cannabinoid receptor, which were not modulated by LPS. The effect of this endotoxin on FAAH was not mediated by AEA-induced activation of cannabinoid receptors. Conversely, the stimulatory action of LPS on AEA levels might be due to inhibition of FAAH, as suggested by the observation that an increase of AFA amounts was also induced by an irreversible FAAH inhibitor. These results suggest that lymphocytes take part in regulating the peripheral endocannabinoid system and endocannabinoid homeostasis. (literal)
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