Increased expression of CSF1 in patients with eosinophilic asthma

Author:

Du Lijuan123ORCID,Tang Lu12ORCID,Xiao Lisha12ORCID,Tang Kun12ORCID,Zeng Zhimin12,Liang Yuxia12ORCID,Guo Yubiao12ORCID

Affiliation:

1. Department of Pulmonary and Critical Care Medicine The First Affiliated Hospital of Sun Yat‐Sen University Guangzhou Guangdong China

2. Institute of Respiratory Diseases of Sun Yat‐Sen University Guangzhou Guangdong China

3. Department of Respiratory and Critical Care Medicine The Affiliated Hospital of Guizhou Medical University Guiyang Guizhou China

Abstract

AbstractBackgroundThe link between colony‐stimulating factor 1 (CSF1) and asthma was reported recently. However, the role and mechanism of CSF1 in asthma remain poorly understood. In this study, we aimed to explore the expression and its potential mechanism of CSF1 in asthma.MethodsCSF1 expression in the airway samples from asthmatics and healthy controls were examined, then the correlations between CSF1 and eosinophilic indicators were analyzed. Subsequently, bronchial epithelial cells (BEAS‐2B) with CSF1 overexpression and knockdown were constructed to investigate the potential molecular mechanism of CSF1. Finally, the effect of CSF1R inhibitor on STAT1 was investigated.ResultsThe expression of CSF1 was significantly increased in patients with asthma compared to healthy controls, especially in patients with severe and eosinophilic asthma. Upregulated CSF1 positively correlated with airway‐increased eosinophil inflammation. In vitro, cytokines interleukin 13 (IL‐13) and IL‐33 can stimulate the upregulation of CSF1 expression. CSF1 overexpression enhanced p‐CSF1R/CSF1R and p‐STAT1/STAT1 expression, while knockdown CSF1 using anti‐CSF1 siRNAs decreased p‐CSF1R/CSF1R and p‐STAT1/STAT1 expression. Furthermore, the inhibitor of CSF1R significantly decreased p‐STAT1/STAT1 expression.ConclusionsSputum CSF1 may be involved in asthmatic airway eosinophil inflammation by interacting with CSF1R and further activating the STAT1 signaling. Interfering this potential pathway could serve as an anti‐inflammatory therapy for asthma.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Guangdong Province

Publisher

Wiley

Subject

Immunology,Immunology and Allergy

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