Alteration in Claudin-4 Contributes to Airway Inflammation and Responsiveness in Asthma
Allergy, Asthma & Immunology Research
;
: 25-33, 2018.
Artigo
em Inglês
| WPRIM
| ID: wpr-739390
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 epithelial 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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Óvulo
/
Plasma
/
Asma
/
Sódio
/
Imunoglobulina E
/
Citocinas
/
RNA Interferente Pequeno
/
Eosinófilos
/
Células Epiteliais
/
Claudinas
Limite:
Animais
/
Humanos
Idioma:
Inglês
Revista:
Allergy, Asthma & Immunology Research
Ano de publicação:
2018
Tipo de documento:
Artigo
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