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

Abstract

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 (CB2) 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 CB2 agonists provide anti-inflammatory effects during acute inflammation and what challenges exist in the translation of CB2 modulating therapeutics into the clinic.

• Authors: Mohammed Tayab Hussain, David R Greaves, Asif Jilani Iqbal
• Journal: DNA and cell biology (DNA Cell Biol) Vol. 38 Issue 10 Pg. 1025-1029 (Oct 2019) ISSN: 1557-7430 [Electronic] United States
• PMID: 31532239 (Publication Type: Journal Article, Review)

Chemical References

• CNR2 protein, human
• Cannabinoid Receptor Agonists
• Cannabinoid Receptor Antagonists
• Cytokines
• Ligands
• Receptor, Cannabinoid, CB2

Topics

• Animals
• Atherosclerosis (drug therapy, genetics, metabolism, pathology)
• Cannabinoid Receptor Agonists (therapeutic use)
• Cannabinoid Receptor Antagonists (therapeutic use)
• Colitis (drug therapy, genetics, metabolism, pathology)
• Cytokines (metabolism, pharmacology)
• Disease Models, Animal
• Gene Expression Regulation
• Humans
• Inflammation
• Ligands
• Mice
• Mice, Knockout
• Multiple Sclerosis (drug therapy, genetics, metabolism, pathology)
• Neutrophil Infiltration
• Neutrophils (drug effects, metabolism, pathology)
• Receptor, Cannabinoid, CB2 (agonists, antagonists & inhibitors, deficiency, genetics)
• Reperfusion Injury (drug therapy, genetics, metabolism, pathology)