Upregulation of the transcription factor GATA-3 in upper airway mucosa after in vivo and in vitro allergen challenge

Citation
Y. Nakamura et al., Upregulation of the transcription factor GATA-3 in upper airway mucosa after in vivo and in vitro allergen challenge, J ALLERG CL, 105(6), 2000, pp. 1146-1152
Citations number
27
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
ISSN journal
00916749 → ACNP
Volume
105
Issue
6
Year of publication
2000
Part
1
Pages
1146 - 1152
Database
ISI
SICI code
0091-6749(200006)105:6<1146:UOTTFG>2.0.ZU;2-E
Abstract
Background: Allergic rhinitis is a complex upper airways disorder character ized by the infiltration of eosinophils and T-H2-type T lymphocytes. GATA-3 is a novel transcription factor recently shown to regulate IL-5 and, possi bly, IL-4 gene expression. We previously reported that GATA-3 is increased within the bronchial mucosa of allergic asthmatic subjects compared with co ntrol subjects. Objective: In the present study we set out to determine whether there is al so an increased number of cells expressing GATA-3 messenger (m)RNA within t he nasal mucosa of patients with allergic rhinitis. Methods: Inferior turbinate biopsy specimens mere obtained from patients wi th allergic rhinitis and nonatopic control subjects before and after local allergen provocation in vivo. To assess the contribution of resident cells expressing GATA-3 mRNA, we also performed isolated explant studies in which nasal mucosal tissue from subjects with allergic rhinitis and nonatopic co ntrol subjects was cultured in allergen-treated medium The presence of mRNA coding for GATA-3, IL-5, IL-4, IL-13, and GM-CSF was assessed by using in situ hybridization. Results: The number of GATA-3 mRNA(+) cells was increased after local aller gen provocation in vivo (increase in GATA-3 mRNA(+) cells [mean +/- SEM]: s ubjects,vith allergic rhinitis, 11.3 +/- 8.7; control subjects, 1.2 +/- 4.1 ; P < .05) and in explanted nasal mucosa in vitro (subjects with allergic r hinitis, 10.2 +/- 3.8; control subjects, 2.7 +/- 4.4; P < .05). The gene ex pression of GATA-3 was significantly correlated to the numbers of IL-5 (r = 0.87) and GM-CSF (r = 0.79) mRNA(+) cells but not with IL-4 or IL-13 mRNA( +) cells. Conclusion: In summary, the expression of the transcription factor GATA-3 w as increased after allergen challenge, and this was evident in the absence of de novo inflammatory cell recruitment. GATA-3 may be a potential target in the treat ment of allergic diseases, such as rhinitis.