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<p>Acute lung injury (ALI) is a common serious complication following deep hypothermic circulatory arrest (DHCA). Monocytes and macrophages play crucial roles in producing inflammatory mediators and regulating innate and adaptive immunity. In our specific rat model of DHCA-induced ALI, we previously showed that autophagy actually has a detrimental effect on lung injury rather than a protective effect. Recently, we reported that monocytes serve an important role in this model. Here, single-cell RNA sequencing was performed on lung tissue cells collected from healthy rats and rats after DHCA. Notably, there was a selective and dramatic increase in the subpopulation of CD43<sup>low</sup> monocytes in the DHCA group, which expressed high levels of CCR5 and exhibited a proinflammatory phenotype. Allosteric CCR5 drug blockade not only reduced CCR5 expression and alleviated lung injury but also, interestingly, inhibited autophagy. These results suggest that the recruitment of CCR5<sup>+</sup> inflammatory monocytes into pulmonary tissue contributes to ALI after DHCA and that blocking CCR5 is a plausible intervention for DHCA-induced lung injury by modulating autophagy.</p>

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Recruitment of CCR5+ inflammatory monocytes in pulmonary tissue contributes to acute lung injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月24日

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  • Dongdong Wei,
  • Xuebiao Li,
  • Guocong Xu,
  • Yupeng Sun,
  • Xian Zhu,
  • Qunjun Duan,
  • Ning Gao,
  • Aiqiang Dong,
  • Minjian Kong

摘要

Acute lung injury (ALI) is a common serious complication following deep hypothermic circulatory arrest (DHCA). Monocytes and macrophages play crucial roles in producing inflammatory mediators and regulating innate and adaptive immunity. In our specific rat model of DHCA-induced ALI, we previously showed that autophagy actually has a detrimental effect on lung injury rather than a protective effect. Recently, we reported that monocytes serve an important role in this model. Here, single-cell RNA sequencing was performed on lung tissue cells collected from healthy rats and rats after DHCA. Notably, there was a selective and dramatic increase in the subpopulation of CD43low monocytes in the DHCA group, which expressed high levels of CCR5 and exhibited a proinflammatory phenotype. Allosteric CCR5 drug blockade not only reduced CCR5 expression and alleviated lung injury but also, interestingly, inhibited autophagy. These results suggest that the recruitment of CCR5+ inflammatory monocytes into pulmonary tissue contributes to ALI after DHCA and that blocking CCR5 is a plausible intervention for DHCA-induced lung injury by modulating autophagy.