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Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis.
J Physiol Pharmacol. 2010 Feb; 61(1):89-97.JP

Abstract

This study was performed to assess whether mice lacking the cannabinoid receptor CB1, CB2 or both receptors show increased susceptibility to TNBS colitis in comparison to wildtype mice. Previously, activation of CB1 and CB2 receptors showed attenuation of TNBS colitis in mice. The aim of the study was to investigate the susceptibility of three mouse strains CB1-, CB2- and CB1+2 double knockout mice in the model of TNBS colitis. The different knockout mice were given each a single enema with TNBS 7 mg, volume 150 microl (in 50% ethanol solution) on day 1. Control group (C57BL/6 mice) received the same concentration of TNBS enema and each strain received vehicle application of 150 microl 50% ethanol solution. After a 3-day period, the animals were sacrificed and their colon excised. A scoring system was used to describe macroscopical and histological changes. Messenger RNA-expression of TNF-alpha and IL-1beta as pro-inflammatory markers was measured by RT-PCR. All three knockout strains showed increased susceptibility to TNBS colitis quantified by macroscopical and histological scoring systems and pro-inflammatory cytokine expression in comparison to the TNBS control group (wild type C57BL/6 animals). Mice lacking the CB1-, CB2-receptor or both receptors showed aggravation of inflammation in the model of TNBS colitis. Lacking of both cannabinoid receptors did not result in potentiation of colitis severity compared to lacking of each CB1 or CB2, respectively. These results suggest that the endocannabinoid system may have tonic inhibitory effects on inflammatory responses in the colon.

Authors+Show Affiliations

First Department of Medicine, University of Erlangen-Nuremberg, Erlangen, Germany. Matthias.Engel@uk-erlangen.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20228420

Citation

Engel, M A., et al. "Mice Lacking Cannabinoid CB1-, CB2-receptors or Both Receptors Show Increased Susceptibility to Trinitrobenzene Sulfonic Acid (TNBS)-induced Colitis." Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, vol. 61, no. 1, 2010, pp. 89-97.
Engel MA, Kellermann CA, Burnat G, et al. Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis. J Physiol Pharmacol. 2010;61(1):89-97.
Engel, M. A., Kellermann, C. A., Burnat, G., Hahn, E. G., Rau, T., & Konturek, P. C. (2010). Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis. Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, 61(1), 89-97.
Engel MA, et al. Mice Lacking Cannabinoid CB1-, CB2-receptors or Both Receptors Show Increased Susceptibility to Trinitrobenzene Sulfonic Acid (TNBS)-induced Colitis. J Physiol Pharmacol. 2010;61(1):89-97. PubMed PMID: 20228420.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis. AU - Engel,M A, AU - Kellermann,C A, AU - Burnat,G, AU - Hahn,E G, AU - Rau,T, AU - Konturek,P C, PY - 2009/04/03/received PY - 2010/01/12/accepted PY - 2010/3/16/entrez PY - 2010/3/17/pubmed PY - 2010/10/5/medline SP - 89 EP - 97 JF - Journal of physiology and pharmacology : an official journal of the Polish Physiological Society JO - J Physiol Pharmacol VL - 61 IS - 1 N2 - This study was performed to assess whether mice lacking the cannabinoid receptor CB1, CB2 or both receptors show increased susceptibility to TNBS colitis in comparison to wildtype mice. Previously, activation of CB1 and CB2 receptors showed attenuation of TNBS colitis in mice. The aim of the study was to investigate the susceptibility of three mouse strains CB1-, CB2- and CB1+2 double knockout mice in the model of TNBS colitis. The different knockout mice were given each a single enema with TNBS 7 mg, volume 150 microl (in 50% ethanol solution) on day 1. Control group (C57BL/6 mice) received the same concentration of TNBS enema and each strain received vehicle application of 150 microl 50% ethanol solution. After a 3-day period, the animals were sacrificed and their colon excised. A scoring system was used to describe macroscopical and histological changes. Messenger RNA-expression of TNF-alpha and IL-1beta as pro-inflammatory markers was measured by RT-PCR. All three knockout strains showed increased susceptibility to TNBS colitis quantified by macroscopical and histological scoring systems and pro-inflammatory cytokine expression in comparison to the TNBS control group (wild type C57BL/6 animals). Mice lacking the CB1-, CB2-receptor or both receptors showed aggravation of inflammation in the model of TNBS colitis. Lacking of both cannabinoid receptors did not result in potentiation of colitis severity compared to lacking of each CB1 or CB2, respectively. These results suggest that the endocannabinoid system may have tonic inhibitory effects on inflammatory responses in the colon. SN - 1899-1505 UR - https://www.unboundmedicine.com/medline/citation/20228420/Mice_lacking_cannabinoid_CB1__CB2_receptors_or_both_receptors_show_increased_susceptibility_to_trinitrobenzene_sulfonic_acid__TNBS__induced_colitis_ L2 - http://www.jpp.krakow.pl/journal/archive/02_10/pdf/89_02_10_article.pdf DB - PRIME DP - Unbound Medicine ER -