Alteration in Claudin-4 Contributes to Airway Inflammation and Responsiveness in Asthma
- Authors
- Lee, Pureun-Haneul; Kim, Byeong-Gon; Lee, Sun-Hye; Lee, June-Hyuck; Park, Sung-Woo; Kim, Do-Jin; Park, Choon-Sik; Leikauf, George D.; Jane, An-Soo
- Issue Date
- Jan-2018
- Publisher
- 대한천식알레르기학회
- Keywords
- Asthma; epithelial barrier; claudin-4
- Citation
- Allergy, Asthma & Immunology Research, v.10, no.1, pp 25 - 33
- Pages
- 9
- Journal Title
- Allergy, Asthma & Immunology Research
- Volume
- 10
- Number
- 1
- Start Page
- 25
- End Page
- 33
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/6358
- DOI
- 10.4168/aair.2018.10.1.25
- ISSN
- 2092-7355
2092-7363
- Abstract
- Purpose: Claudin-4 has been reported to function as a paracellular sodium barrier and is one of the 3 major claudins expressed in lung alveolar epithelia) cells. However, the possible role of claudin-4 in bronchial asthma has not yet been fully studied. In this study, we aimed to elucidate the role of claudin-4 in the pathogenesis of bronchial asthma. Methods: We determined claudin-4 levels in blood from asthmatic patients. Moreover, using mice sensitized and challenged with OVA, as well as sensitized and challenged with saline, we investigated whether claudin-4 is involved in the pathogenesis of bronchial asthma. Der p1 induced the inflammatory cytokines in NHBE cells. Results: We found that claudin-4 in blood from asthmatic patients was increased compared with that from healthy control subjects. Plasma claudin-4 levels were significantly higher in exacerbated patients than in control patients with bronchial asthma. The plasma claudin-4 level was correlated with eosinophils, total IgE, FEV1% pred, and FEV1/FVC. Moreover, lung tissues from the OVA-OVA mice showed significant increases in transcripts and proteins of claudin-4 as well as in TJ breaks and the densities of claudin-4 staining. When claudin-4 was knocked down by transfecting its siRNA, inflammatory cytokine expressions, which were induced by Der p1 treatment, were significantly increased. Conclusions: These findings thus raise the possibility that regulation of lung epithelial barrier proteins may constitute a therapeutic approach for asthma.
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Collections - College of Medicine > Department of Internal Medicine > 1. Journal Articles
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