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Endocannabinoid receptor CB2R is significantly expressed in aspirin‐exacerbated respiratory disease: a pilot study
Author(s) -
Corrado Alessia,
Battle Monica,
Wise Sarah K.,
Lee F. EunHyung,
Guidot David M.,
DelGaudio John M.,
Molina Samuel A.,
Levy Joshua M.
Publication year - 2018
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.22163
Subject(s) - endocannabinoid system , medicine , nasal polyps , cannabinoid receptor , receptor , asthma , immunology , endocrinology , agonist
Background The endocannabinoid system represents a highly conserved, innate signaling network with direct and indirect control of eicosanoid‐mediated inflammation. Activation of the type 2 cannabinoid receptor (CB2R) leads to decreased type 2 inflammation and reduced production of arachidonic acid (AA). Given that altered AA metabolism is associated with aspirin‐exacerbated respiratory disease (AERD), we hypothesized that expression of the CB2R gene CNR2 is increased in AERD. Methods Nasal polyps from consecutive patients undergoing endoscopic sinus surgery for AERD or allergic fungal rhinosinusitis (AFRS) were prospectively evaluated. Control sphenoid mucosa was collected from patients undergoing endoscopic skull base procedures. Expression and localization of endocannabinoid receptors were evaluated by quantitative reverse transcript–polymerase chain reaction (qRT‐PCR) and immunohistochemistry. A 2‐group unpaired t test with unequal variances was used to evaluate group differences. Results Thirteen subjects were included in this pilot study, including 5 controls, 5 AFRS patients, and 3 AERD patients. Upregulated expression of CNR2 was detected in subjects with AERD vs both AFRS ( p = 0.049) and controls ( p = 0.047), with a mean increase of 5.2‐fold. No significant differences in expression of the CB1R gene CNR1 were detected between control and AFRS groups. Immunohistochemistry predominantly localized CB1R and CB2R expression to the surface epithelium in all subjects. Conclusion The endocannabinoid system is an emerging immunomodulatory network that may be involved in AERD. This is the first study of CB2R in sinonasal disease, showing significantly increased transcription in nasal polyps from subjects with AERD. Additional study is warranted to further evaluate the contribution and therapeutic potential of this novel finding in chronic rhinosinusitis.