| First Author | Tschöp J | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 1 | Pages | 499-505 |
| PubMed ID | 19525393 | Mgi Jnum | J:150038 |
| Mgi Id | MGI:3849612 | Doi | 10.4049/jimmunol.0900203 |
| Citation | Tschop J, et al. (2009) The cannabinoid receptor 2 is critical for the host response to sepsis. J Immunol 183(1):499-505 |
| abstractText | Leukocyte function can be modulated through the cannabinoid receptor 2 (CB2R). Using a cecal ligation and puncture (CLP) model of sepsis, we examined the role of the CB2R during the immune response to an overwhelming infection. CB2R-knock out (KO) mice showed decreased survival as compared with wild-type mice. CB2R-KO mice also had increased serum IL-6 and bacteremia. Twenty-four hours after CLP, the CB2R-deficient mice had increased lung injury. Additionally, CB2R-deficiency led to increased neutrophil recruitment, decreased neutrophil activation, and decreased p38 activity at the site of infection. Consistent with a novel role for CB2R in sepsis, CB2R-agonist treatment in wild-type mice increased the mean survival time in response to CLP. Treatment with CB2R-agonist also decreased serum IL-6 levels, bacteremia, and damage to the lungs compared with vehicle-treated mice. Finally, the CB2R agonist decreased neutrophil recruitment, while increasing neutrophil activation and p38 activity at the site of infection compared with vehicle-treated mice. These data suggest that CB2R is a critical regulator of the immune response to sepsis and may be a novel therapeutic target. |
