Mechanisms of inflammatory cell attachment in chronic relapsing experimental allergic encephalomyelitis: A scanning and high-voltage electron microscopic study of the injured mouse blood-brain barrier

• Published in: Microvascular research Vol. 41; no. 3; pp. 299 - 310
• Main Authors: Lossinsky, A.S., Pluta, R., Song, M.J., Badmajew, V., Moretz, R.C., Wisniewski, H.M.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.05.1991; Elsevier
• Subjects: Animals; Biological and medical sciences; Blood-Brain Barrier; Brain - blood supply; Brain - ultrastructure; Cell Adhesion; Chronic Disease; Encephalomyelitis, Autoimmune, Experimental - pathology; Female; Lymphocytes - pathology; Lymphocytes - ultrastructure; Medical sciences; Mice; Microscopy, Electron, Scanning; Monocytes - pathology; Monocytes - ultrastructure; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Neurology; Recurrence; Spinal Cord - blood supply; Spinal Cord - ultrastructure; Scanning electron microscopy; Animal model; Multiple sclerosis; Nervous system diseases; Encephalomyelitis; Rodentia; Autoimmune disease; Blood brain barrier; Inflammatory disease; Vertebrata; High voltage electron microscopy; Experimental disease; Mammalia; Mouse; Ultrastructure; Animal; Blood vessel
• ISSN: 0026-2862; 1095-9319
• DOI: 10.1016/0026-2862(91)90030-F

Brain and spinal cord blood vessels from mice subjected to chronic relapsing experimental allergic encephalomyelitis were examined by scanning (SEM) and high-voltage electron microscopy (HVEM). SEM analysis of veins and venules from affected tissue regions demonstrated inflammatory cells (ICs), primarily lymphocytes or monocytes, attached to the luminal endothelial cell (EC) surface adjacent to the junctional complexes. In transverse section these cells were shown by HVEM to extend and to insert filopodia (lymphocytes) or flap-like lamellapodia (monocytes) into the luminal EC surfaces. Affected ECs often expressed increased microvillar projection as well as parajunctional crater-like structures on their luminal surfaces. Based on scanning and high-voltage electron microscopy, we present morphological evidence that some populations of sensitized ICs do not penetrate the EC junctions initially during EC attachment but instead insert pseudopodial projections into specialized openings in the ECs that are formed in response to chronic inflammation.