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Accumulation of CRTH2-positive leukocytes in human allergic nasal mucosa.

Authors: Shirasaki, H  Kikuchi, M  Kanaizumi, E  Himi, T 
Citation: Shirasaki H, etal., Ann Allergy Asthma Immunol. 2009 Feb;102(2):110-5.
Pubmed: (View Article at PubMed) PMID:19230460
DOI: Full-text: DOI:10.1016/S1081-1206(10)60239-6

BACKGROUND: Prostaglandin D2 (PGD2) has been thought to be a potent mediator involved in allergic rhinitis because PGD2 has been recovered from the nasal lavage fluid of patients with allergic rhinitis after allergen provocation and because PGD2 receptor antagonists relieved nasal allergic symptoms in an animal model of allergic rhinitis. The inflammatory effects of PGD2 are exerted through high-affinity interactions with 2 G protein-coupled receptors: D-prostanoid receptor 1 and chemoattractant-homologous receptor expressed on TH2 cells (CRTH2). CRTH2 may mediate the recruitment of leukocytes during a nasal allergic response. OBJECTIVE: To evaluate the number of CRTH2-expressing cells in allergic and nonallergic human nasal mucosa by means of immunohistochemical analysis. METHODS: Human turbinates were obtained after turbinectomy from 14 patients with nasal obstruction refractory to medical therapy. To identify cells expressing the CRTH2 protein, double immunostaining was performed using anti-CRTH2 antibody and monoclonal anti-leukocyte antibodies. RESULTS: The immunohistochemical study revealed that anti-CRTH2 antibody labeled eosinophils, macrophages, mast cells, T lymphocytes, epithelial cells, and submucosal glands in the nasal mucosa. CRTH2 expressions of these leukocytes in allergic nasal mucosa are significantly up-regulated compared with those in nonallergic nasal mucosa. CONCLUSION: These results suggest that CRTH2 may play an important role in the recruitment of leukocytes into allergic nasal mucosa.


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RGD Object Information
RGD ID: 5135021
Created: 2011-07-08
Species: All species
Last Modified: 2011-07-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.