S100A9 in adult asthmatic patients: a biomarker for neutrophilic asthma

Quang Luu Quoc; Youngwoo Choi; Tra Cao Thi Bich; Eun-Mi Yang; Yoo Seob Shin; Hae Sim Park

doi:10.1038/s12276-021-00652-5

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자료유형: 학술저널

저자정보: Quang Luu Quoc (Ajou University School of Medicine) Youngwoo Choi (Ajou University School of Medicine) Tra Cao Thi Bich (Ajou University School of Medicine) Eun-Mi Yang (Ajou University School of Medicine) Yoo Seob Shin (Ajou University School of Medicine) Hae Sim Park (Ajou University School of Medicine)

저널정보: 대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제53권

발행연도: 2021.7

수록면: 1 - 10 (10page)

DOI: 10.1038/s12276-021-00652-5

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The biomarkers and therapeutic targets of neutrophilic asthma (NA) are poorly understood. Although S100 calcium-binding protein A9 (S100A9) has been shown to correlate with neutrophil activation, its role in asthma pathogenesis has not been clarified. This study investigated the mechanism by which S100A9 is involved in neutrophil activation, neutrophil extracellular trap (NET)-induced airway inflammation, and macrophage polarization in NA. The S100A9 levels (by ELISA) in sera/culture supernatant of peripheral blood neutrophils (PBNs) and M0 macrophages from asthmatic patients were measured and compared to those of healthy controls (HCs). The function of S100A9 was evaluated using airway epithelial cells (AECs) and PBNs/M0 macrophages from asthmatic patients, as well as a mouse asthma model. The serum levels of S100A9 were higher in NA patients than in non-NA patients, and there was a positive correlation between serum S100A9 levels and sputum neutrophil counts (r = 0.340, P = 0.005). Asthmatic patients with higher S100A9 levels had lower PC20 methacholine values and a higher prevalence of severe asthma (SA) (P < .050). PBNs/M0 macrophages from SA released more S100A9 than those from non-SA patients. PBNs from asthmatic patients induced S100A9 production by AECs, which further activated AECs via the extracellular signal-regulated kinase (ERK) pathway, stimulated NET formation, and induced M1 macrophage polarization. Higher S100A9 levels in sera, bronchoalveolar lavage fluid, and lung tissues were observed in the mouse model of NA but not in the other mouse models. These results suggest that S100A9 is a potential serum biomarker and therapeutic target for NA.

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