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. 2021 May 5;11:9616. doi: 10.1038/s41598-021-89032-7

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© The Author(s) 2021

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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PTX3 depletion did not modify brain inflammatory response at 5 weeks after TBI. Astrocytes (A, GFAP), brain myeloid cells (B, CD11b; C, CD68) and collagen deposition (E, by sirius red) were quantified in the quantified in the ipsilateral (il)-cortex within the first 350 μm from the edge of the contusion showing no difference between WT and PTX3 KO. Axonal loss in contralateral (cl)-corpus callosum and external capsule (D, by luxol fast blue) did not differ between the two strains. Data is presented as mean ± SEM, n = 5 (TBI WT/PTX3 KO). Unpaired t-test = ns.