Cellular neuroscienceEarly infiltration of CD8+ macrophages/microglia to lesions of rat traumatic brain injury
Section snippets
Animal experiments
Lewis rats (8–9 weeks of age, 350–400 g, Elevage Janvier, Le Genest-St-Isle, France) were housed with equal daily periods of light and dark and free access to food and water. All procedures were performed in accordance with the published International Health Guidelines under a protocol approved by the Administration District Official Committee. The number of rats used and their suffering were minimized.
TBI was induced using a weight-drop contusion model in anesthetized rats according to a
TBI-induced cortical injury
TBI by weight drop is a well-established animal model for brain trauma studies and was reported to generate a reproducible injury in the ipsilateral cortex. Here the development of the lesion following TBI was analyzed using HE staining. Selective neuronal loss and necrotic loci in the impacted somatosensory cortex was seen 12 h post-TBI using microscopy. Coagulation necrosis (pannecrosis), where no neuronal structure can be observed, was seen 2 days post-injury in ipsilateral somatosensory
Discussion
We have analyzed early accumulation of CD8+ macrophages/microglia in rat brains up to 96 h after TBI induced by weight-drop contusion. Significant CD8+ cell accumulation was observed 3 days post-TBI and increased steadily. The CD8+ cells were strictly distributed to areas of pannecrosis and mainly accumulated at the edge of the pannecrosis. The morphology, time course and distribution of CD8+ cells were similar to reactive ED1+ and EMAPII+ macrophages/microglia, but different from few
Conclusion
In conclusion, we report the early recruitment of activated CD8+ macrophages in rat TBI induced by weight-drop contusion. These activated CD8+ phagocytes are mainly distributed to the border of pannecrosis. The abundance of this subpopulation and their strategic location suggest that they might have a role in early lesion formation and probably CD8+ macrophages could be a suitable target for the development of immunotherapeutic, anti-inflammatory agents in TBI.
Acknowledgments
This work has been supported in part by the BMBF.
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