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  • 1
    ISSN: 1432-0533
    Keywords: Key words Meningitis ; C5a complement ; Macrophage ; Astrocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Subarachnoidal application of the complement C5a fragment was used to induce acute experimental meningitis in rabbits and rats within 30–60 min. The early stages of the cellular inflammatory response were studied by means of flow cytometry, transmission electron microscopy and immunofluorescence microscopy. Infiltration of polymorphonuclear leukocytes (PMN) into the subarachnoidal space was the earliest event of the inflammatory reaction. By morphological criteria we found that PMN interacted with cells of the mononuclear-macrophage lineage (MML) and the marginal astrocytes via pseudopodia, whereas the pial cells were not involved in early stages of the inflammatory response. The number of invaded MML that were positive with the ED2 marker increased, indicating the hematogenous origin of the immigrating cell population. PMN were found to infiltrate the perivascular space of the marginal arterial vessel segments. This perivascular infiltration was assumed to be the first manifestation of cerebral vasculitis. The intimate association of resident cerebral cells (astrocytes) with invading PMN and MML is suggestive of a transient interaction of these cell types.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Meningitis ; C5a complement ; Macrophage ; Astrocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Subarachnoidal application of the complement C5a fragment was used to induce acute experimental meningitis in rabbits and rats within 30–60 min. The early stages of the cellular inflammatory response were studied by means of flow cytometry, transmission electron microscopy and immunofluorescence microscopy. Infiltration of polymorphonuclear leukocytes (PMN) into the subarachnoidal space was the earliest event of the inflammatory reaction. By morphological criteria we found that PMN interacted with cells of the mononuclear-macrophage lineage (MML) and the marginal astrocytes via pseudopodia, whereas the pial cells were not involved in early stages of the inflammatory response. The number of invaded MML that were positive with the ED2 marker increased, indicating the hematogenous origin of the immigrating cell population. PMN were found to infiltrate the perivascular space of the marginal arterial vessel segments. This perivascular infiltration was assumed to be the first manifestation of cerebral vasculitis. The intimate association of resident cerebral cells (astrocytes) with invading PMN and MML is suggestive of a transient interaction of these cell types.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 242 (1985), S. 399-407 
    ISSN: 1432-0878
    Keywords: Cerebral microvasculature ; Inflammatory reaction ; Polymorphonuclear leukocytes ; α-Bungarotoxin ; Cat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Postcapillary venules represent the segment of the microvasculature most vulnerable to inflammatory processes. While there is a considerable body of data on the peripheral vasculature, little is known about the primary events occurring during inflammatory reactions in cererbral blood vessels. We introduce here a model by which the migration of polymorphonuclear leukocytes through the CNS endothelial barrier can be studied. Alpha-bungarotoxin is used as a chemotactic agent and is shown, for the first time, to act by activating the complement cascade. Leukocytes migrate through the endothelium transcellularly. Two modes of migration are described: (i) a direct mode whereby the cells use temporary pores in the vessel wall as portals, and (ii) an indirect mode whereby the leukocytes leave the vascular compartment after being enveloped by and incorporated into endothelial cells. The functional implications of these findings lead us to conclude that the direct mode of migration is a causal agent in the massive breakdown of the blood-brain barrier under acute inflammatory conditions.
    Type of Medium: Electronic Resource
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