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. 2021 Aug 11;9:693342. doi: 10.3389/fcell.2021.693342

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Copyright © 2021 Hu, Li, Wang, Chen, Qian and Dai.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Toll-like receptor 4 (TLR4) deficiency ameliorates neuronal damage and improves neurological dysfunction. (A–C) Double immunofluorescence staining showed the triggering receptor expressed on myeloid cells 2 (TREM2)/CD68-positive cells in the cortex and hippocampus after subarachnoid hemorrhage (SAH). (D–F) Nissl staining and quantitative number of survived neurons. (G) Comparison of the escape latency on the navigation test on days 1, 2, 3, 4, 5, and 7. The SAH models were performed on day 6. (H) Comparison of the time spent in the target quadrant after removal of the platform on day 7. These data are shown as mean ± SEM (TLR4-TREM2: Knocking down the TREM2 in the TLR4-KO mice; *p<0.05, **p<0.01, ***p<0.001, ***p<0.001, ****p<0.001, ^#p<0.001; scale bar = 25 μm).