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β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury.

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Title: β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury.
Authors: Li, Lei, Peng, Ruilong, Wang, Cong, Chen, Xin, Gheyret, Dilmurat, Guan, Siyu, Chen, Bo, Liu, Yafan, Liu, Xilei, Cao, Yiyao, Han, Cha, Xiong, Jianhua, Li, Fanjian, Lu, Taoyuan, Jia, Haoran, Li, Kaiji, Wang, Jinchao, Zhang, Xu, Xu, Jianye, Wang, Yajuan
Source: Cell Communication & Signaling; 2/8/2025, Vol. 23 Issue 1, p1-21, 21p
Subject Terms: CD54 antigen, MEDICAL sciences, BRAIN injuries, INFLAMMATORY mediators, TREATMENT effectiveness, NEUTROPHILS
Abstract: Neutrophils are the first responders among peripheral immune cells to infiltrate the central nervous system following a traumatic brain injury (TBI), triggering neuroinflammation that can exacerbate secondary tissue damage. The precise molecular controls that dictate the inflammatory behavior of neutrophils post-TBI, however, remain largely elusive. Our comprehensive analysis of the molecular landscape surrounding the trauma in TBI mice has revealed a significant alteration in the abundance of β2 integrin (ITGB2), predominantly expressed by neutrophils and closely associated with immune responses. Using the fluid percussion injury (FPI) mouse model, we investigated the therapeutic efficacy of Rovelizumab, an agent that blocks ITGB2. The treatment has demonstrated significant improvements in neurologic function in TBI mice, attenuating blood–brain barrier permeability, mitigating oxidative stress and inflammatory mediator release, and enhancing cerebral perfusion. Moreover, ITGB2 blockade has effectively limited the adherence, migration, and infiltration of neutrophils, and has impeded the formation of neutrophil extracellular traps (NETs) upon their activation. Finally, it was demonstrated that ITGB2 mediates these effects mainly through its interaction with intercellular adhesion molecule-1 (ICAM 1) of endotheliocyte. These findings collectively illuminate ITGB2 as a crucial molecular switch that governs the adverse effects of neutrophils post-TBI and could be targeted to improve clinical outcome in patients. [ABSTRACT FROM AUTHOR]
Copyright of Cell Communication & Signaling is the property of BioMed Central and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Complementary Index
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  Data: β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury.
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  Data: <searchLink fieldCode="AR" term="%22Li%2C+Lei%22">Li, Lei</searchLink><br /><searchLink fieldCode="AR" term="%22Peng%2C+Ruilong%22">Peng, Ruilong</searchLink><br /><searchLink fieldCode="AR" term="%22Wang%2C+Cong%22">Wang, Cong</searchLink><br /><searchLink fieldCode="AR" term="%22Chen%2C+Xin%22">Chen, Xin</searchLink><br /><searchLink fieldCode="AR" term="%22Gheyret%2C+Dilmurat%22">Gheyret, Dilmurat</searchLink><br /><searchLink fieldCode="AR" term="%22Guan%2C+Siyu%22">Guan, Siyu</searchLink><br /><searchLink fieldCode="AR" term="%22Chen%2C+Bo%22">Chen, Bo</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Yafan%22">Liu, Yafan</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Xilei%22">Liu, Xilei</searchLink><br /><searchLink fieldCode="AR" term="%22Cao%2C+Yiyao%22">Cao, Yiyao</searchLink><br /><searchLink fieldCode="AR" term="%22Han%2C+Cha%22">Han, Cha</searchLink><br /><searchLink fieldCode="AR" term="%22Xiong%2C+Jianhua%22">Xiong, Jianhua</searchLink><br /><searchLink fieldCode="AR" term="%22Li%2C+Fanjian%22">Li, Fanjian</searchLink><br /><searchLink fieldCode="AR" term="%22Lu%2C+Taoyuan%22">Lu, Taoyuan</searchLink><br /><searchLink fieldCode="AR" term="%22Jia%2C+Haoran%22">Jia, Haoran</searchLink><br /><searchLink fieldCode="AR" term="%22Li%2C+Kaiji%22">Li, Kaiji</searchLink><br /><searchLink fieldCode="AR" term="%22Wang%2C+Jinchao%22">Wang, Jinchao</searchLink><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Xu%22">Zhang, Xu</searchLink><br /><searchLink fieldCode="AR" term="%22Xu%2C+Jianye%22">Xu, Jianye</searchLink><br /><searchLink fieldCode="AR" term="%22Wang%2C+Yajuan%22">Wang, Yajuan</searchLink>
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  Data: Cell Communication & Signaling; 2/8/2025, Vol. 23 Issue 1, p1-21, 21p
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  Data: <searchLink fieldCode="DE" term="%22CD54+antigen%22">CD54 antigen</searchLink><br /><searchLink fieldCode="DE" term="%22MEDICAL+sciences%22">MEDICAL sciences</searchLink><br /><searchLink fieldCode="DE" term="%22BRAIN+injuries%22">BRAIN injuries</searchLink><br /><searchLink fieldCode="DE" term="%22INFLAMMATORY+mediators%22">INFLAMMATORY mediators</searchLink><br /><searchLink fieldCode="DE" term="%22TREATMENT+effectiveness%22">TREATMENT effectiveness</searchLink><br /><searchLink fieldCode="DE" term="%22NEUTROPHILS%22">NEUTROPHILS</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Neutrophils are the first responders among peripheral immune cells to infiltrate the central nervous system following a traumatic brain injury (TBI), triggering neuroinflammation that can exacerbate secondary tissue damage. The precise molecular controls that dictate the inflammatory behavior of neutrophils post-TBI, however, remain largely elusive. Our comprehensive analysis of the molecular landscape surrounding the trauma in TBI mice has revealed a significant alteration in the abundance of β2 integrin (ITGB2), predominantly expressed by neutrophils and closely associated with immune responses. Using the fluid percussion injury (FPI) mouse model, we investigated the therapeutic efficacy of Rovelizumab, an agent that blocks ITGB2. The treatment has demonstrated significant improvements in neurologic function in TBI mice, attenuating blood–brain barrier permeability, mitigating oxidative stress and inflammatory mediator release, and enhancing cerebral perfusion. Moreover, ITGB2 blockade has effectively limited the adherence, migration, and infiltration of neutrophils, and has impeded the formation of neutrophil extracellular traps (NETs) upon their activation. Finally, it was demonstrated that ITGB2 mediates these effects mainly through its interaction with intercellular adhesion molecule-1 (ICAM 1) of endotheliocyte. These findings collectively illuminate ITGB2 as a crucial molecular switch that governs the adverse effects of neutrophils post-TBI and could be targeted to improve clinical outcome in patients. [ABSTRACT FROM AUTHOR]
– Name: Abstract
  Label:
  Group: Ab
  Data: <i>Copyright of Cell Communication & Signaling is the property of BioMed Central and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1186/s12964-025-02071-9
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