Fig. 4

Factor XII enhances inflammatory processes after traumatic brain injury. a Determination of CCL2 protein concentrations in the brain tissue of sham-operated mice and mice treated with rHA-Infestin-4 or vehicle 2, 6, and 12 h, and 1 day (d1) after injury (n = 4–5 per group, ***P < 0.001, one-way ANOVA followed by Bonferroni multiple comparison test). b Quantification of CCL2 concentrations in the brain tissue of FXII^−/− mice, sham-operated mice, and wildtype controls 12 h and 1 day (d1) after injury (n = 4–5 per group, ***P < 0.001, **P < 0.01, *P < 0.05, one-way ANOVA followed by Bonferroni multiple comparison test compared with WT mice)^−/−. c Relative gene expression of CCL2 in the injured cortices of FXII-deficient mice and wildtype controls, and rHA-Infestin-4- and vehicle-treated mice on day 1 after trauma induction (n = 5 per group, *P < 0.05, unpaired, two-tailed Student’s t test, amount of gene expression normalized to sham-operated animals (not shown)). d Macrophages and activated microglia were quantified in the lesioned hemispheres after 1 (d1) and 3 days (d3) after brain trauma (left). Representative immunohistochemical stainings of CD11b-positive macrophages/microglia in FXII-deficient animals and wildtype mice on d1 (right). Scale bar depicts 100 μm (n = 4, ***P < 0.001, **P < 0.01, *P < 0.05, unpaired, two-tailed Student’s t test)