TY  - JOUR
AU  - YANG, Zhe
AU  - DUAN, Min
AU  - YE, Yumeng
AU  - WANG, Yongyi
AU  - ZHANG, Jiao
AU  - WANG, Xuejia
AU  - WANG, Jun
AU  - LI, Yang
PY  - 2025
TI  - Effects of myeloid cell-specific knockout of G-CSFR on the progression of acute radiation pneumonitis in mice
JO  - Military Medical Sciences
SN  - 1674-9960
SP  - 582
EP  - 588
VL  - 49
IS  - 8
AB  - ObjectiveTo investigate the impact of myeloid cell-specific knockout of the granulocyte colony-stimulating factor receptor (G-CSFR) on the progression of acute radiation pneumonitis.MethodsMyeloid cell-specific G-CSFR knockout (G-CSFR-/-, Lyz2-cre) mice were constructed. G-CSFR-/-, Lyz2-cre and C57BL/6N mice underwent a single whole-body irradiation with 6.5 Gy of 60Co γ-rays to establish a model of radiation injury. The lung function of mice was assessed using a mouse lung function test system at 3, 7 and 14-days post γ-ray irradiation. Pathological changes in the lung tissue were analyzed via hematoxylin and eosin (HE) staining of paraffin sections. Tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) levels were measured via radioimmunoassay. IL-8 and its receptor CXCR2 were quantified using enzyme-linked immunosorbent assay (ELISA). The infiltration of neutrophils in lung tissue was evaluated by immunohistochemical detection of myeloperoxidase.ResultsAt 3-, 7- and 14-days post-irradiation with 6.5 Gy of 60Co γ-rays, there were no significant differences observed in lung function or interstitial inflammatory lesions between G-CSFR-/-, Lyz2-cre mice and C57BL/6N mice. However, the infiltration of neutrophils in lung tissue of G-CSFR-/-, Lyz2-cre mice was significantly reduced (P＜0.01), and the levels of IL-8, CXCR2 and TNF-α in lung tissues were markedly lower than in C57BL/6N mice (P＜0.05).ConclusionThe myeloid cell-specific knockout of G-CSFR can effectively diminish neutrophil infiltration as well as inflammatory cytokine levels in lung tissues following radiation exposure.
UR  - https://doi.org/10.7644/j.issn.1674-9960.2025.08.004
DO  - 10.7644/j.issn.1674-9960.2025.08.004