C-type lectin Mincle initiates IL-17-mediated inflammation in acute exacerbations of idiopathic pulmonary fibrosis

Chen Tao; He Xian; Zhou Nian-yu; Song Jia-cui; Weng Dong; Li Hui-ping

Biomedicine & Pharmacotherapy (Mar 2023)

C-type lectin Mincle initiates IL-17-mediated inflammation in acute exacerbations of idiopathic pulmonary fibrosis

Chen Tao,
He Xian,
Zhou Nian-yu,
Song Jia-cui,
Weng Dong,
Li Hui-ping

Affiliations

Chen Tao: Department of Respiratory Medicine, School of Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China; Department of Respiratory Medicine, People’s Hospital of Deyang City, Sichuan Province, China
He Xian: Department of Respiratory Medicine, School of Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China
Zhou Nian-yu: Department of Respiratory Medicine, School of Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China
Song Jia-cui: Department of Respiratory Medicine, School of Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China
Weng Dong: Department of Respiratory Medicine, School of Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China; Correspondence to: 507 Zheng Min Road, Shanghai 200433, China.
Li Hui-ping: Department of Respiratory Medicine, School of Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China; Correspondence to: 507 Zheng Min Road, Shanghai 200433, China.

Journal volume & issue: Vol. 159
p. 114253

Abstract

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Rationale: Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) has a poor prognosis and high mortality. However, there is limited information regarding the mechanisms of AE-IPF. Aims: We aimed to explore the function of macrophage-inducible C-type lectin (Mincle) in AE-IPF. Methods: In the present study, Mincle was detected in the lung tissues of AE-IPF patients. Mincle-deficient (Mincle-/-) mice and wild-type C57BL/6 mice were administered bleomycin (BLM), followed by HSV1 viral infection to establish the AE-IPF model. Results: Mincle was increased in the lung tissues of AE-IPF patients compared with those with stable IPF (P = 0.04) and healthy controls (P = 0.009). The survival rate of the Mincle-/-+BLM+HSV group was higher than that of the WT+BLM+HSV group. The mice in the Mincle-/-+BLM+HSV group exhibited milder inflammation and lower acute lung injury scores (P = 0.008). Mincle was expressed on inflammatory monocytes and neutrophils (CD11b+Gr1 +F4/80-) and monocyte-derived macrophages (Mo-AMs, CD11b+Gr1 +F4/80 +) in the BALF of AE-IPF mice. Mo-AMs were significantly increased in the WT+BLM+HSV group compared with the WT+BLM+PBS (P < 0.0001) and Mincle-/-+BLM+HSV (P = 0.0009) groups. Deletion of Mincle decreased the proportion of Th17 cells and Mo-AMs in the Mincle-/-+BLM+HSV group. Conclusions: Mincle contributed to acute inflammation in AE-IPF by promoting Th17 differentiation.

Published in Biomedicine & Pharmacotherapy

ISSN: 0753-3322 (Print); 1950-6007 (Online)
Publisher: Elsevier
Country of publisher: France
LCC subjects: Medicine: Therapeutics. Pharmacology
Website: https://www.journals.elsevier.com/biomedicine-and-pharmacotherapy

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