Sterile inflammation after permanent distal MCA occlusion in hypertensive rats.
The pathophysiology of stroke is governed by immune reactions within and remote from the injured brain. Hypertension, a major cause and comorbidity of stroke, entails systemic vascular inflammation and may influence poststroke immune responses. This aspect is, however, underestimated in previous studies. Here we aimed to delineate the sequence of cellular inflammation after stroke in spontaneously hypertensive (SH) rats. Spontaneously hypertensive rats were subjected to permanent middle cerebral artery occlusion and killed after 1 or 4 days. Immune cells of the peripheral blood and those which have infiltrated the injured brain were identified and quantified by flow cytometry. The spatial distribution of myeloid cells and T lymphocytes, and the infarct volume were assessed by histology. We observed a concerted infiltration of immune cells into the ischemic brain of SH rats. At day 1, primarily neutrophils, monocytes, macrophages, and myeloid dendritic cells entered the brain, whereas the situation at day 4 was dominated by microglia, macrophages, lymphatic dendritic cells, and T cells. Postischemic inflammation did not cause secondary tissue damage during the subacute stage of experimental stroke in SH rats. Considering the intrinsic vascular pathology of SH rats, our study validates this strain for further translational research in poststroke inflammation.
1] Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany [2] Institute of Veterinary Anatomy, University of Leipzig, Leipzig, Germany.
Karoline
K
Möller
1] Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany [2] Translational Centre for Regenerative Medicine, University of Leipzig, Leipzig, Germany [3] Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Johannes
J
Boltze
Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Claudia
C
Pösel
Institute of Veterinary Anatomy, University of Leipzig, Leipzig, Germany.
Johannes
J
Seeger
IDT Biologika GmbH, Dessau-Rosslau, Germany.
Tobias
T
Stahl
1] Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany [2] Translational Centre for Regenerative Medicine, University of Leipzig, Leipzig, Germany.
Daniel-Christoph
DC
Wagner
D000818:Animals; D001921:Brain / Q000098:blood supply / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D003713:Dendritic Cells / Q000378:metabolism / Q000473:pathology*; D006973:Hypertension / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology*; D017628:Microglia / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D011918:Rats, Inbred SHR