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. 2022 Apr 15;12:6289. doi: 10.1038/s41598-022-10419-1

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Microglial activation and process illustration. (A) According to the “Old Paradigm”, resting microglia are stimulated by a stimulus, such as a TBI, and proceed to become “Activated” along the “Canonical” or “Alternative” activation pathways to become either “M1” pro-inflammatory microglia with a specific surface marker profile, or “M2” anti-inflammatory microglia with a different surface marker phenotype. (B) In the “New Paradigm”, microglia are activated across a spectrum of pro- and anti-inflammatory activities and capable of expressing many combinations of surface markers according to cellular functions and not tied to a single pro- or anti-inflammatory phenotype. (C) We used cluster identification algorithms to find unique populations present in controlled cortical impact injured rats compared to sham-injured controls. These clusters were then characterized on the basis of their unique surface marker features. Finally, the changes in the distribution of microglia in each subpopulation was determined over time in both ipsilateral and contralateral hemispheres (simulated data displayed).