Change of connexin 37 in allergen-induced airway inflammation.
- Author:
Seoung Ju PARK
1
;
Kyung Sun LEE
;
So Ri KIM
;
Kyung Hoon MIN
;
Ka Young LEE
;
Yeong Hun CHOE
;
Seung Yong PARK
;
Sang Hyun HONG
;
Yong Chul LEE
Author Information
1. Department of Internal Medicine and Airway Remodeling Laboratory, Chonbuk National University Medical School, Jeonju 561-180, Korea. leeyc@chonbuk.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
asthma;
connexin 37;
epithelial cells;
gap junctions;
inflammation mediators;
models, animal;
respiratory system
- MeSH:
Airway Resistance;
Allergens/toxicity;
Animals;
Asthma/etiology/genetics/immunology/*metabolism;
Base Sequence;
Bronchoalveolar Lavage Fluid/cytology;
Cell Adhesion Molecules/metabolism;
Cells, Cultured;
Chemokines/metabolism;
Connexins/genetics/*metabolism;
Cytokines/metabolism;
DNA Primers/genetics;
Disease Models, Animal;
Epithelial Cells/metabolism;
Female;
Lung/immunology/metabolism/pathology;
Mice;
Mice, Inbred C57BL;
Ovalbumin/immunology/toxicity;
RNA, Messenger/genetics/metabolism;
Trachea/metabolism
- From:Experimental & Molecular Medicine
2007;39(5):629-640
- CountryRepublic of Korea
- Language:English
-
Abstract:
Gap junction channels formed with connexins directly link to the cytoplasm of adjacent cells and have been implicated in intercellular signaling. Connexin 37 (Cx37) is expressed in the gas-exchange region of the lung. Recently, Cx37 has been reported to be involved in the pathogenesis of inflammatory disease. However, no data are available on the role of Cx37 in allergic airway inflammatory disease. In the present study, we used a murine model of ovalbumin (OVA)-induced allergic airway disease and primary murine epithelial cells to examine the change of Cx37 in allergic airway disease. These mice develop the following typical pathophysiological features of asthma: airway hyperresponsiveness, airway inflammation, and increased IL-4, IL-5, IL-13, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, eotaxin, and RANTES levels in lungs. Cx37 protein and mRNA expression were decreased in OVA-induced allergic airway disease. Immunoreactive Cx37 localized in epithelial layers around the bronchioles in control mice, which dramatically disappeared in allergen-induced asthmatic lungs. Moreover, the levels of Cx37 protein in lung tissues showed significantly negative correlations with airway inflammation, airway responsiveness, and levels of Th2 cytokines in lungs. These findings indicate that change of Cx37 may be associated with the asthma phenotype.
