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Targeted deletion of cannabinoid receptors CB1 and CB2 produced enhanced inflammatory responses to influenza A/PR/8/34 in the absence and presence of Delta9-tetrahydrocannabinol.
J Leukoc Biol. 2008 Mar; 83(3):785-96.JL

Abstract

We have previously reported that Delta-9-tetrahydrocannabinol (Delta(9)-THC)-treated mice challenged with influenza virus A/PR/8/34 (PR8) developed increased viral hemagglutinin 1 (H1) mRNA levels and decreased monocyte and lymphocyte recruitment to the pulmonary airways when compared with mice challenged with PR8 alone. The objective of the present study was to examine the role of cannabinoid (CB(1)/CB(2)) receptors in mediating the effects of Delta(9)-THC on immune and epithelial cell responses to PR8. In the current study, Delta(9)-THC-treated CB(1)/CB(2) receptor null (CB(1)-/-/CB(2)-/-) and wild-type mice infected with PR8 had marked increases in viral H1 mRNA when compared with CB(1)-/-/CB(2)-/- and wild-type mice challenged with PR8 alone. However, the magnitude of the H1 mRNA levels was greatly reduced in CB(1)-/-/CB(2)-/- mice as compared with wild-type mice. In addition, Delta(9)-THC-treated CB(1)-/-/CB(2)-/- mice infected with PR8 had increased CD4+ T cells and IFN-gamma in bronchoalveolar lavage fluid with greater pulmonary inflammation when compared with Delta(9)-THC-treated wild-type mice infected with PR8. Delta(9)-THC treatment of CB(1)-/-/CB(2)-/- mice in the presence or absence of PR8 challenge also developed greater amounts of mucous cell metaplasia in the affected bronchiolar epithelium. Collectively, the immune and airway epithelial cell responses to PR8 challenge in Delta(9)-THC-treated CB(1)-/-/CB(2)-/- and wild-type mice indicated the involvement of CB(1)/CB(2) receptor-dependent and -independent mechanisms.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, and Center for Integrative Toxicology, Michigan State University, East Lansing, MI 48824-1317, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18073275

Citation

Buchweitz, John P., et al. "Targeted Deletion of Cannabinoid Receptors CB1 and CB2 Produced Enhanced Inflammatory Responses to Influenza A/PR/8/34 in the Absence and Presence of Delta9-tetrahydrocannabinol." Journal of Leukocyte Biology, vol. 83, no. 3, 2008, pp. 785-96.
Buchweitz JP, Karmaus PW, Williams KJ, et al. Targeted deletion of cannabinoid receptors CB1 and CB2 produced enhanced inflammatory responses to influenza A/PR/8/34 in the absence and presence of Delta9-tetrahydrocannabinol. J Leukoc Biol. 2008;83(3):785-96.
Buchweitz, J. P., Karmaus, P. W., Williams, K. J., Harkema, J. R., & Kaminski, N. E. (2008). Targeted deletion of cannabinoid receptors CB1 and CB2 produced enhanced inflammatory responses to influenza A/PR/8/34 in the absence and presence of Delta9-tetrahydrocannabinol. Journal of Leukocyte Biology, 83(3), 785-96.
Buchweitz JP, et al. Targeted Deletion of Cannabinoid Receptors CB1 and CB2 Produced Enhanced Inflammatory Responses to Influenza A/PR/8/34 in the Absence and Presence of Delta9-tetrahydrocannabinol. J Leukoc Biol. 2008;83(3):785-96. PubMed PMID: 18073275.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeted deletion of cannabinoid receptors CB1 and CB2 produced enhanced inflammatory responses to influenza A/PR/8/34 in the absence and presence of Delta9-tetrahydrocannabinol. AU - Buchweitz,John P, AU - Karmaus,Peer W F, AU - Williams,Kurt J, AU - Harkema,Jack R, AU - Kaminski,Norbert E, Y1 - 2007/12/11/ PY - 2007/12/13/pubmed PY - 2008/5/15/medline PY - 2007/12/13/entrez SP - 785 EP - 96 JF - Journal of leukocyte biology JO - J Leukoc Biol VL - 83 IS - 3 N2 - We have previously reported that Delta-9-tetrahydrocannabinol (Delta(9)-THC)-treated mice challenged with influenza virus A/PR/8/34 (PR8) developed increased viral hemagglutinin 1 (H1) mRNA levels and decreased monocyte and lymphocyte recruitment to the pulmonary airways when compared with mice challenged with PR8 alone. The objective of the present study was to examine the role of cannabinoid (CB(1)/CB(2)) receptors in mediating the effects of Delta(9)-THC on immune and epithelial cell responses to PR8. In the current study, Delta(9)-THC-treated CB(1)/CB(2) receptor null (CB(1)-/-/CB(2)-/-) and wild-type mice infected with PR8 had marked increases in viral H1 mRNA when compared with CB(1)-/-/CB(2)-/- and wild-type mice challenged with PR8 alone. However, the magnitude of the H1 mRNA levels was greatly reduced in CB(1)-/-/CB(2)-/- mice as compared with wild-type mice. In addition, Delta(9)-THC-treated CB(1)-/-/CB(2)-/- mice infected with PR8 had increased CD4+ T cells and IFN-gamma in bronchoalveolar lavage fluid with greater pulmonary inflammation when compared with Delta(9)-THC-treated wild-type mice infected with PR8. Delta(9)-THC treatment of CB(1)-/-/CB(2)-/- mice in the presence or absence of PR8 challenge also developed greater amounts of mucous cell metaplasia in the affected bronchiolar epithelium. Collectively, the immune and airway epithelial cell responses to PR8 challenge in Delta(9)-THC-treated CB(1)-/-/CB(2)-/- and wild-type mice indicated the involvement of CB(1)/CB(2) receptor-dependent and -independent mechanisms. SN - 0741-5400 UR - https://www.unboundmedicine.com/medline/citation/18073275/Targeted_deletion_of_cannabinoid_receptors_CB1_and_CB2_produced_enhanced_inflammatory_responses_to_influenza_A/PR/8/34_in_the_absence_and_presence_of_Delta9_tetrahydrocannabinol_ L2 - https://doi.org/10.1189/jlb.0907618 DB - PRIME DP - Unbound Medicine ER -