2. Academic Validation
  3. Mac-1/ICAM-1-dependent trogocytosis contributes to ICAM-1hi neutrophils-induced lung injury in traumatic brain injury

Mac-1/ICAM-1-dependent trogocytosis contributes to ICAM-1hi neutrophils-induced lung injury in traumatic brain injury

  • Int Immunopharmacol. 2025 Jul 31:163:115276. doi: 10.1016/j.intimp.2025.115276.
Zhimin Zou 1,  Yin Lu 2,  Zhili Liang 3,  Jiahui Fu 4,  Jiazhuo Liu 5,  Qin Li 6,  Marc Maegele 7,  Qiaobing Huang 8,  Li Li 9,  Zhengtao Gu 10
Affiliations

Affiliations

  • 1 Department of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, Guangdong, China; Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China; Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: zzm9190@smu.edu.cn.
  • 2 Department of Neurosurgery, Zhongnan Hospital, Wuhan University, Wuhan, Hubei 430030, China. Electronic address: ly12138@smu.edu.cn.
  • 3 Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: zlleung@163.com.
  • 4 Department of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, Guangdong, China; Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China. Electronic address: gloria0203@smu.edu.cn.
  • 5 Department of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, Guangdong, China; Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China. Electronic address: ljz22210523@smu.edu.cn.
  • 6 Department of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, Guangdong, China; Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China. Electronic address: joy5915@smu.edu.cn.
  • 7 Department of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, Guangdong, China; Institute for Research in Operative Medicine (IFOM), University Witten/Herdecke (UW/H), Campus Cologne-Merheim, Ostmerheimerstr. 200, D-51109 Köln, Germany; Department for Trauma and Orthopedic Surgery, Cologne-Merheim Medical Center (CMMC), University Witten/Herdecke (UW/H), Campus Cologne-Merheim, Ostmerheimerstr. 200, D-51109 Köln, Germany. Electronic address: Marc.Maegele@t-online.de.
  • 8 Guangdong Provincial Key Lab of Shock and Microcirculation, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: bing@smu.edu.cn.
  • 9 Department of Emergency Medicine, General Hospital of Southern Theater Command, PLA, Guangzhou, Guangdong 510010, China; Department of Trauma and War Wound Center, General Hospital of Southern Theater Command, PLA, Guangzhou, Guangdong 510010, China. Electronic address: li435319585@smu.edu.cn.
  • 10 Department of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, Guangdong, China; Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China. Electronic address: yytao700@smu.edu.cn.
PMID: 40749609 DOI: 10.1016/j.intimp.2025.115276
Abstract

The lung is the most vulnerable organ following traumatic brain injury (TBI) and lung injury is closely associated with poor prognosis in patients. Recent studies have highlighted the role of neutrophils with high ICAM-1 expression (ICAM-1hi) in lung injury. These cells exhibit enhanced migration capacity and pro-inflammatory functions, might play a major role in the development of acute pulmonary failure following brain injury. This study aimed to investigate the potential role of ICAM-1hi neutrophils in TBI-induced lung injury and elucidate the underlying mechanisms of ICAM-1hi phenotype formation. In the TBI rat model, we found that a large number of neutrophils with ICAM-1hi phenotype and upregulated neutrophil Elastase were present not only in the contused brain but also in the injured lungs. Further analysis in vitro model revealed that trogocytosis, a Mac-1/ICAM-1-dependent process by which neutrophils capture membrane fragments containing ICAM-1 from contacted endothelial cells, contributes to neutrophils acquiring the ICAM-1hi phenotype. Moreover, we found that S100B, significantly elevated in TBI rat serum, can induce the ICAM-1 expression in endothelial cells and facilitate the trogocytosis between neutrophils and endothelial cells in a Mac-1/ICAM-1-dependent manner. Finally, we found that both ICAM-1 blockade and S100B inhibition significantly reduce the number of ICAM-1hi neutrophils in the lungs and alleviated lung injury following TBI. Taken together, these results suggest that by targeting S100B and Mac-1/ICAM-1-dependent trogocytosis, it may be an effective therapeutic potential to reduce the population of ICAM-1hi neutrophils and thus improve lung injury after TBI.

Keywords

ICAM-1(hi) neutrophil; Secondary lung injury; Traumatic brain injury; Trogocytosis.

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