Single-Cell Transcriptome Analysis of Radiation Pneumonitis Mice
Miaomiao Yang,
Qiang Fan,
Tom K. Hei,
Guodong Chen,
Wei Cao,
Gang Meng,
Wei Han
Affiliations
Miaomiao Yang
Anhui Province Key Laboratory of Medical Physics and Technology/Institute of Health and Medical Technology, Hefei Institutes of Physical Sciences, Chinese Academy of Sciences, Hefei 230031, China
Qiang Fan
Anhui Province Key Laboratory of Medical Physics and Technology/Institute of Health and Medical Technology, Hefei Institutes of Physical Sciences, Chinese Academy of Sciences, Hefei 230031, China
Tom K. Hei
Center for Radiological Research, College of Physician and Surgeons, Columbia University Medical Center, New York, NY 10032, USA
Guodong Chen
Anhui Province Key Laboratory of Medical Physics and Technology/Institute of Health and Medical Technology, Hefei Institutes of Physical Sciences, Chinese Academy of Sciences, Hefei 230031, China
Wei Cao
Anhui Province Key Laboratory of Medical Physics and Technology/Institute of Health and Medical Technology, Hefei Institutes of Physical Sciences, Chinese Academy of Sciences, Hefei 230031, China
Gang Meng
Clinical Pathology Center, The Fourth Affiliated Hospital of Anhui Medical University, Hefei 230022, China
Wei Han
Anhui Province Key Laboratory of Medical Physics and Technology/Institute of Health and Medical Technology, Hefei Institutes of Physical Sciences, Chinese Academy of Sciences, Hefei 230031, China
Radiation-induced lung injury (RILI), especially radiation pneumonitis (RP), is a common clinical complication associated with thoracic radiotherapy for malignant tumors. However, the specific contributions of each cell subtype to this process are unknown. Here, we provide the single-cell pathology landscape of the RP in a mouse model by unbiased single-cell RNA-seq (scRNA-seq). We found a decline of type 2 alveolar cells in the RP lung tissue, with an expansion of macrophages, especially the Fabp4low and Spp1high subgroup, while Fabp4high macrophages were almost depleted. We observed an elevated expression of multiple mitochondrial genes in the RP group, indicating a type 2 alveolar cell (AT2) response to oxidative stress. We also calculated the enrichment of a cGAS-STING signaling pathway, which may be involved in regulating inflammatory responses and cancer progression in AT2 cells of PR mice. We delineate markers and transcriptional states, identify a type 2 alveolar cell, and uncover fundamental determinants of lung fibrosis and inflammatory response in RP lung tissue of mice.
