Abstract
Traumatic brain injury (TBI) is complex and involves multiple processes that contribute to functional decline. Progressive neuropathies result from delayed cellular death following the initial impact. Although the precise mechanisms responsible for delayed injury are unknown, numerous data implicate a role for the peripheral immune system in perpetuating neuroinflammation after TBI. A previous report demonstrated that splenic CCL20 chemokine expression was upregulated 24 h after lateral fluid percussive impact (LFPI), prior to neuronal expression but consistent with neurodegeneration. Here, we expand on those data to report increased CCL20 protein expression in white matter 48 h after LFPI and demonstrate that CCL20 is directly toxic to primary neurons and oligodendrocytes subjected to oxygen glucose deprivation. The temporal expression profile of CCL20, coupled with in vitro toxicity to primary cells, suggests that this chemokine exerts deleterious effects on cell viability following TBI. These findings warrant further investigations into the use of CCL20 as a potential biomarker and/or therapeutic target.
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Acknowledgments
This work was supported by NIH RO1 NS052839. We want to thank Dr. Christopher Katnik and Jesus Recio for their effort with the primary neuronal cultures. There are no conflicts of interest.
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Leonardo, C.C., Musso, J., Das, M. et al. CCL20 Is Associated with Neurodegeneration Following Experimental Traumatic Brain Injury and Promotes Cellular Toxicity In Vitro. Transl. Stroke Res. 3, 357–363 (2012). https://doi.org/10.1007/s12975-012-0203-8
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DOI: https://doi.org/10.1007/s12975-012-0203-8