The Impact of Cannabinoid Receptor 2 Deficiency on Neutrophil Recruitment and Inflammation

• Published in: DNA and cell biology Vol. 38; no. 10; p. 1025
• Main Authors: Hussain, Mohammed Tayab, Greaves, David R, Iqbal, Asif Jilani
• Format: Journal Article
• Language: English
• Published: United States 01-10-2019
• Subjects: Animals; Atherosclerosis - drug therapy; Atherosclerosis - genetics; Atherosclerosis - metabolism; Atherosclerosis - pathology; Cannabinoid Receptor Agonists - therapeutic use; Cannabinoid Receptor Antagonists - therapeutic use; Colitis - drug therapy; Colitis - genetics; Colitis - metabolism; Colitis - pathology; Cytokines - metabolism; Cytokines - pharmacology; Disease Models, Animal; Gene Expression Regulation; Humans; Inflammation; Ligands; Mice; Mice, Knockout; Multiple Sclerosis - drug therapy; Multiple Sclerosis - genetics; Multiple Sclerosis - metabolism; Multiple Sclerosis - pathology; Neutrophil Infiltration; Neutrophils - drug effects; Neutrophils - metabolism; Neutrophils - pathology; Receptor, Cannabinoid, CB2 - agonists; Receptor, Cannabinoid, CB2 - antagonists & inhibitors; Receptor, Cannabinoid, CB2 - deficiency; Receptor, Cannabinoid, CB2 - genetics; Reperfusion Injury - drug therapy; Reperfusion Injury - genetics; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; cannabinoids; cannabinoid receptors; inflammation; neutrophils
• DOI: 10.1089/dna.2019.5024
• EISSN: 1557-7430

Neutrophil trafficking into damaged or infected tissues is essential for the initiation of inflammation, clearance of pathogens and damaged cells, and ultimately tissue repair. Neutrophil recruitment is highly dependent on the stepwise induction of adhesion molecules and promigratory chemokines and cytokines. A number of studies in animal models have shown the efficacy of cannabinoid receptor 2 (CB
) agonists in limiting inflammation in a range of preclinical models of inflammation, including colitis, atherosclerosis, multiple sclerosis, and ischemia-reperfusion injury. Recent work in preclinical models of inflammation raises two questions: by what mechanisms do CB
agonists provide anti-inflammatory effects during acute inflammation and what challenges exist in the translation of CB
modulating therapeutics into the clinic.