T-lymphocyte infiltration in the brain parenchyma is a hallmark of acute neuroinflammation following subarachnoid hemorrhage in mice

Subarachnoid hemorrhage (SAH) triggers neuroinflammation including the recruitment and activation of immune cells. T-cells in particular, have been shown to promote the evolution of secondary injury following ischemic stroke, however their role in SAH is still unclear.In this study we aimed to evaluate T-cells’ recruitment in the brain of SAH-injured mice to next investigate their specific role in injury progression.Adult C57BL/6J mice were subjected to SAH by blood injection in the prechiasmatic cistern or sham procedure and sacrificed at 3 or 7 days-post-injury (dpi). Sensorimotor deficits were longitudinally evaluated by Garcia modified test up to 7-dpi. Diffusion weighted imaging (DWI) was performed at 3-dpi. Brain histopathology was performed at 3 and 7-dpi. Gene expression was assessed by RT-PCR in the hippocampus and lesion area at 7-dpi.SAH mice displayed sensorimotor deficits up to 7-dpi. The DWI analysis at 3-dpi showed increased hyperintense areas close to the lesion, indicating the presence of vasogenic edema. Infiltration of CD3+ T-cells was observed in the lesion of SAH mice only and was associated with increased neuronal death and IBA1 stained area in the lesion and in the hippocampus. The gene expression analysis showed increased levels of specific lymphocytic and microglial genes in the same areas at 7-dpi.SAH induced functional impairment and neuroinflammation characterized by vasogenic edema and microglial activation associated with T-cells’ infiltration in brain parenchyma. Further studies will aim to better elucidate T-cells’ contribution to injury evolution following SAH and to attribute it to specific phenotypes.