Fast microglial activation after severe traumatic brain injuries
- PDF / 1,378,950 Bytes
- 7 Pages / 595.276 x 790.866 pts Page_size
- 6 Downloads / 176 Views
SHORT COMMUNICATION
Fast microglial activation after severe traumatic brain injuries Julia Lier 1 & Benjamin Ondruschka 2 & Ingo Bechmann 1 & Jan Dreßler 2 Received: 18 February 2020 / Accepted: 22 April 2020 # The Author(s) 2020
Abstract Traumatic brain injury is among the leading causes of death in individuals under 45 years of age. However, since trauma mechanisms and survival times differ enormously, the exact mechanisms leading to the primary and secondary injury and eventually to death after traumatic brain injury (TBI) remain unclear. Several studies showed the versatile functions of microglia, the innate macrophages of the brain, following a TBI. Earlier being characterized as rather neurotoxic, neuroprotective capacities were recently demonstrated, therefore, making microglia one of the key players following TBI. Especially in cases with only short survival times, immediate microglial reactions are of great forensic interest in questions of wound age estimation. Using standardized immunohistochemical methods, we examined 8 cases which died causatively of TBI with survival times between minutes and 7 days and 5 control cases with cardiovascular failure as the cause of death to determine acute changes in microglial morphology and antigen expression after TBI. In this pilot study, we detected highly localized changes in microglial morphology already early after traumatic damage, e.g., activated microglia and phagocyted erythrocytes in the contusion areas in cases with minute survival. Furthermore, an altered antigen expression was observed with increasing trauma wound age, showing similar effects like earlier transcriptomic studies. There is minute data on the direct impact of shear forces on microglial morphology. We were able to show localization-depending effects on microglial morphology causing localized dystrophy and adjacent activation. While rodent studies are widespread, they fail to mimic the exact mechanisms in human TBI response. Therefore, more studies focusing on cadaveric samples need to follow to thoroughly define the mechanisms leading to cell destruction and eventually evaluate their forensic value. Keywords Chronic traumatic encephalopathy . Immunohistochemistry . Inflammation . Microglia . Traumatic brain injury
Introduction Traumatic brain injuries (TBI) have a biphasic course [1]. While tissue destruction and necrosis occur immediately and directly at the impact zone together with intracranial or intracerebral hemorrhages as well as cortical contusions (primary Julia Lier and Benjamin Ondruschka contributed equally to this work as first authors Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00414-020-02308-x) contains supplementary material, which is available to authorized users. * Benjamin Ondruschka [email protected] 1
Institute of Anatomy, University of Leipzig, Liebigstraße 13, D-04103 Leipzig, Germany
2
Institute of Legal Medicine, University of Leipzig, Johannisallee 28, D-04103 Leipzig, Germany
phase),
Data Loading...
