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Tschöp, J.* ; Kasten, K.R.* ; Nogueiras, R.* ; Goetzman, H.S.* ; Cave, C.M.* ; England, L.G.* ; Dattilo, J.* ; Lentsch, A.B.* ; Tschöp, M.H.* ; Caldwell, C.C.*

The cannabinoid receptor 2 is critical for the host response to sepsis.

J. Immunol. 183, 499-505 (2009)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
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.
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Publication type Article: Journal article
Document type Scientific Article
ISSN (print) / ISBN 0022-1767
e-ISSN 1550-6606
Quellenangaben Volume: 183, Issue: 1, Pages: 499-505 Article Number: , Supplement: ,
Publisher American Association of Immunologists
Reviewing status Peer reviewed