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Elevated S100A4 in asthmatics and an allergen‐induced mouse asthma model

The elevated S100A4 level has been found in some inflammatory diseases. However, the expression and role of S100A4 in asthma is unknown. The expression of S100A4 in induced sputum and plasma from healthy control and asthmatics were assessed by ELISA. Then an allergen‐induced asthma mouse model treat...

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Published in:Journal of cellular biochemistry 2019-06, Vol.120 (6), p.9667-9676
Main Authors: Huang, Xiaolin, Qu, Dongming, Liang, Yue, Huang, Qinghua, Li, Mengze, Hou, Changchun
Format: Article
Language:English
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Summary:The elevated S100A4 level has been found in some inflammatory diseases. However, the expression and role of S100A4 in asthma is unknown. The expression of S100A4 in induced sputum and plasma from healthy control and asthmatics were assessed by ELISA. Then an allergen‐induced asthma mouse model treatment with anti‐S100A4 antibody was used to explore the role of S100A4 in the pathogenesis of asthma. The S100A4 levels in sputum not in plasma in asthmatics were significantly increased than those of healthy controls and were negatively correlated with some lung function parameters and were positively correlated with sputum eosinophilia and lymphocyte. The expression of S100A4 in the lung as well as in BALF were also significantly higher in the asthma mouse model and treatment with anti‐S100A4 antibody exhibited reductions in inflammatory cell accumulation, inflammatory mediators, and airway hyper‐responsiveness. We further showed that LY294002, a specific inhibitor of PI3K, markedly decreased S100A4 expression in lung and S100A4 secretion in BALF in asthmatic mice. In conclusion, these data demonstrated that S100A4 may be involved in the pathogenesis of airway inflammation in asthma. We found that elevated sputum S100A4 levels in asthmatics are associated with disease severity and anti‐S100A4 antibody administration resulted in decreased eosinophilic allergic airway inflammation in an OVA‐induced acute asthma model. Our study suggests that S100A4 may participate in the pathogenesis of asthma.
ISSN:0730-2312
1097-4644
DOI:10.1002/jcb.28245