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C1-Inhibitor protects from focal brain trauma in a cortical cryolesion mice model by reducing thrombo-inflammation

Please always quote using this URN: urn:nbn:de:bvb:20-opus-119263
  • Traumatic brain injury (TBI) induces a strong inflammatory response which includes blood-brain barrier damage, edema formation and infiltration of different immune cell subsets. More recently, microvascular thrombosis has been identified as another pathophysiological feature of TBI. The contact-kinin system represents an interface between inflammatory and thrombotic circuits and is activated in different neurological diseases. C1-Inhibitor counteracts activation of the contact-kinin system at multiple levels. We investigated the therapeuticTraumatic brain injury (TBI) induces a strong inflammatory response which includes blood-brain barrier damage, edema formation and infiltration of different immune cell subsets. More recently, microvascular thrombosis has been identified as another pathophysiological feature of TBI. The contact-kinin system represents an interface between inflammatory and thrombotic circuits and is activated in different neurological diseases. C1-Inhibitor counteracts activation of the contact-kinin system at multiple levels. We investigated the therapeutic potential of C1-Inhibitor in a model of TBI. Male and female C57BL/6 mice were subjected to cortical cryolesion and treated with C1-Inhibitor after 1 h. Lesion volumes were assessed between day 1 and day 5 and blood-brain barrier damage, thrombus formation as well as the local inflammatory response were determined post TBI. Treatment of male mice with 15.0 IU C1-Inhibitor, but not 7.5 IU, 1 h after cryolesion reduced lesion volumes by ~75% on day 1. This protective effect was preserved in female mice and at later stages of trauma. Mechanistically, C1-Inhibitor stabilized the blood-brain barrier and decreased the invasion of immune cells into the brain parenchyma. Moreover, C1-Inhibitor had strong antithrombotic effects. C1-Inhibitor represents a multifaceted anti-inflammatory and antithrombotic compound that prevents traumatic neurodegeneration in clinically meaningful settings.show moreshow less

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Metadaten
Author: Christine Albert-Weissenberger, Stine Mencl, Michael K. Schuhmann, Irmak Salur, Eva Göb, Friederike Langhauser, Sarah Hopp, Nelli Hennig, Sven G. Meuth, Marc W. Nolte, Anna-Leena Sirén, Christoph Kleinschnitz
URN:urn:nbn:de:bvb:20-opus-119263
Document Type:Journal article
Faculties:Medizinische Fakultät / Neurochirurgische Klinik und Poliklinik
Medizinische Fakultät / Neurologische Klinik und Poliklinik
Language:English
Parent Title (English):Frontiers in Cellular Neuroscience
ISSN:1662-5102
Year of Completion:2014
Volume:8
Pagenumber:269
Source:Frontiers in Cellular Neuroscience 8:269. doi: 10.3389/fncel.2014.00269
DOI:https://doi.org/10.3389/fncel.2014.00269
Pubmed Id:http://www.ncbi.nlm.nih.gov/pubmed?term=25249935
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Tag:C1-inhibitor; blood-brain barrier; contact-kinin system; edema; inflammation; thrombosis; traumatic brain injury
Release Date:2015/10/20
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung