Endocannabinoid degradation, endotoxic shock and inflammation.

M. Maccarrone, M. Bari, N. Battista, A. Finazzi-Agrò

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Endocannabinoids are an emerging class of lipid mediators, which include amides and esters of long chain polyunsaturated fatty acids. Anandamide (N-arachidonoylethanolamine, AEA) and 2-arachidonoylglycerol (2-AG) are the main endogenous agonists of cannabinoid receptors. Endotoxic shock is a potentially lethal failure of multiple organs that can be initiated by the inflammatory agent lipopolysaccharide (LPS), present in the outer membrane of gram-negative bacteria. LPS has been recently shown to stimulate the production of AEA in rat macrophages, and of 2-AG in rat platelets. The mechanism responsible for this effect has not been elucidated. On the other hand, mast cells are multifunctional bone marrow-derived cells found in mucosal and connective tissues and in the nervous system, where they play an essential role in inflammation. As yet, little is known about endogenous modulators and mechanisms of mast cell activation. Here, we review recent literature on the role of endocannabinoids in endotoxic shock and inflammation, and report our recent research on the effects of LPS on the production of AEA and 2-AG in human lymphocytes, and on AEA degradation by a specific AEA membrane transporter (AMT) and an AEA-degrading enzyme (fatty acid amide hydrolase, FAAH). We also report the ability of the HMC-1 human mast cells to degrade AEA through a nitric oxide-sensitive AMT and a FAAH. The role of endocannabinoids in HMC-1 degranulation is discussed as well. Taken together, it can be suggested that human lymphocytes and mast cells take part in regulating the peripheral endocannabinoid system, which can affect some activities of these cells.

Original languageEnglish
Pages (from-to)53-63
Number of pages11
JournalCurrent Drug Targets: Inflammation and Allergy
Volume1
Issue number1
Publication statusPublished - Mar 2002

Fingerprint

Endocannabinoids
Septic Shock
Inflammation
Mast Cells
Lipopolysaccharides
Membrane Transport Proteins
Lymphocytes
Cannabinoid Receptor Agonists
Multiple Organ Failure
N-arachidonoylethanolamine
Gram-Negative Bacteria
Unsaturated Fatty Acids
Amides
Bone Marrow Cells
Connective Tissue
Nervous System
Nitric Oxide
Esters
Mucous Membrane
Blood Platelets

ASJC Scopus subject areas

  • Immunology and Allergy
  • Pharmacology
  • Immunology

Cite this

Endocannabinoid degradation, endotoxic shock and inflammation. / Maccarrone, M.; Bari, M.; Battista, N.; Finazzi-Agrò, A.

In: Current Drug Targets: Inflammation and Allergy, Vol. 1, No. 1, 03.2002, p. 53-63.

Research output: Contribution to journalArticle

Maccarrone, M. ; Bari, M. ; Battista, N. ; Finazzi-Agrò, A. / Endocannabinoid degradation, endotoxic shock and inflammation. In: Current Drug Targets: Inflammation and Allergy. 2002 ; Vol. 1, No. 1. pp. 53-63.
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