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Epithelial SERPINB10, a novel marker of airway eosinophilia in asthma, contributes to allergic airway inflammation.
- Source :
-
American journal of physiology. Lung cellular and molecular physiology [Am J Physiol Lung Cell Mol Physiol] 2019 Jan 01; Vol. 316 (1), pp. L245-L254. Date of Electronic Publication: 2018 Nov 01. - Publication Year :
- 2019
-
Abstract
- Serine peptidase inhibitor, clade B, member 10 (SERPINB10) expression is increased in IL-13-stimulated human bronchial epithelial cells and in a murine model of allergic airway inflammation. However, the role of SERPINB10 in asthma remains unknown. We examined the association between epithelial SERPINB10 expression and airway eosinophilia in subjects with asthma and the role of Serpinb10 in allergic airway inflammation in an animal model. Epithelial SERPINB10 mRNA and protein expression were markedly increased in subjects with asthma ( n = 60) compared with healthy controls ( n = 25). Epithelial SERPINB10 mRNA levels were significantly correlated with airway hyperresponsiveness (AHR) and three parameters reflecting airway eosinophilia including the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa, and fraction of exhaled nitric oxide in subjects with asthma. Moreover, epithelial SERPINB10 expression was strongly correlated with the epithelial gene signature ( CLCA1, POSTN, and SERPINB2) for type 2 status. In normal human bronchial epithelial cells cultured at air-liquid interface, knockdown of SERPINB10 suppressed IL-13-stimulated periostin (encoded by POSTN) and CCL26 (eotaxin-3) expression by inhibiting the activation of p38 MAPK. Epithelial CCL26 mRNA levels were correlated with SERPINB10 expression in subjects with asthma. Airway knockdown of Serpinb10 alleviated AHR, airway eosinophilia and the expression of periostin and Ccl26 in a murine model of allergic airway disease. Taken together, epithelial SERPINB10 is a novel marker for airway eosinophilia in asthma. Epithelial SERPINB10 contributes to allergic airway eosinophilic inflammation, at least in part, by regulating the expression of periostin and CCL26.
- Subjects :
- Adult
Animals
Asthma pathology
Bronchi pathology
Cell Adhesion Molecules biosynthesis
Cell Adhesion Molecules genetics
Chemokine CCL26 biosynthesis
Chemokine CCL26 genetics
Disease Models, Animal
Eosinophils metabolism
Eosinophils pathology
Epithelial Cells pathology
Female
Gene Knockdown Techniques
Humans
Inflammation metabolism
Inflammation pathology
Male
Mice
Pulmonary Eosinophilia pathology
Serpins genetics
Asthma metabolism
Bronchi metabolism
Epithelial Cells metabolism
Pulmonary Eosinophilia metabolism
Serpins metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1522-1504
- Volume :
- 316
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- American journal of physiology. Lung cellular and molecular physiology
- Publication Type :
- Academic Journal
- Accession number :
- 30382768
- Full Text :
- https://doi.org/10.1152/ajplung.00362.2017