Locally organised and activated Fth1hi neutrophils aggravate inflammation of acute lung injury in an IL-10-dependent manner

Kun Wang, Muyun Wang, Ximing Liao, Shaoyong Gao, Jing Hua, Xiaodong Wu, Qian Guo, Wujian Xu, Jiaxing Sun, Yanan He, Qiang Li () and Wei Gao ()
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Kun Wang: Tongji University School of Medicine
Muyun Wang: Tongji University School of Medicine
Ximing Liao: Tongji University School of Medicine
Shaoyong Gao: Tongji University School of Medicine
Jing Hua: Tongji University School of Medicine
Xiaodong Wu: Tongji University School of Medicine
Qian Guo: Tongji University School of Medicine
Wujian Xu: Tongji University School of Medicine
Jiaxing Sun: Tongji University School of Medicine
Yanan He: Tongji University School of Medicine
Qiang Li: Tongji University School of Medicine
Wei Gao: Tongji University School of Medicine

Nature Communications, 2022, vol. 13, issue 1, 1-19

Abstract: Abstract Acute respiratory distress syndrome (ARDS) is a common respiratory critical syndrome with no effective therapeutic intervention. Neutrophils function in the overwhelming inflammatory process of acute lung injury (ALI) caused by ARDS; however, the phenotypic heterogeneity of pulmonary neutrophils in ALI/ARDS remains largely unknown. Here, using single-cell RNA sequencing, we identify two transcriptionally and functionally heterogeneous neutrophil populations (Fth1hi Neu and Prok2hi Neu) with distinct locations in LPS-induced ALI mouse lungs. Exposure to LPS promotes the Fth1hi Neu subtype, with more inflammatory factors, stronger antioxidant, and decreased apoptosis under the regulation of interleukin-10. Furthermore, prolonged retention of Fth1hi Neu within lung tissue aggravates inflammatory injury throughout the development of ALI/ARDS. Notably, ARDS patients have high ratios of Fth1 to Prok2 expression in pulmonary neutrophils, suggesting that the Fth1hi Neu population may promote the pathological development and provide a marker of poor outcome.

Date: 2022
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DOI: 10.1038/s41467-022-35492-y

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