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  • 1
    Electronic Resource
    Electronic Resource
    Granulocytes in the subarachnoid space of humans and rabbits with bacterial meningitis undergo apoptosis and are eliminated by macrophages (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 472-480 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cell death ; Inflammation ; Leukocytes ; Central nervous system ; Streptococcus pneumoniae
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The contribution of leukocyte apoptosis to the resolution of meningeal inflammation in bacterial meningitis was studied in the cerebrospinal fluid (CSF) and in meningeal infiltrates of humans and rabbits by in situ tailing, flow cytometry, agarose gel electrophoresis, and electron microscopy. In humans, the rate of apoptotic granulocytes was 21.0 ± 20.8% (n = 11) in cytocentrifuge preparations and 3.3 ± 3.4 (n = 14) in putride infiltrates of autopsy cases (P = 0.02). In rabbits, CSF pleocytosis peaked 8 h after the initiation of antibiotic treatment (5311 ± 3122/μl). At this time, the rate of apoptotic granulocytes was 15.2 ± 7.3% in CSF and 1.8 ± 1.4% in the meningeal infiltrates (each group n = 6, P = 0.007). Thereafter, the rate of apoptotic granulocytes in CSF declined below 10%. In humans and rabbits, bands representing internucleosomal fragments of approximately 180 base pairs and multiples thereof were documented on agarose gels. Phagocytosis of apoptotic granulocytes by macrophages was visualized by light and electron microscopy. In conclusion, during resolution of subarachnoid space inflammation in bacterial meningitis, a substantial fraction of granulocytes undergoes apoptosis. These granulocytes are removed by phagocytosis by macrophages. Apoptosis is more frequent in granulocytes floating in the CSF than in adherent cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050921
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  • 2
    Electronic Resource
    Electronic Resource
    In situ demonstration of T cell activation and elimination in the peripheral nervous system during experimental autoimmune neuritis in the Lewis rat (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 360-367 
    Details
    ISSN: 1432-0533
    Keywords: Key words Apoptosis ; Peripheral nervous system ; Experimental autoimmune neuritis ; Guillain-Barré-Strohl syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanisms of activation and termination of autoimmune responses are poorly understood. We have studied the sites and mode of activation and elimination of T cells in actively induced experimental autoimmune neuritis (EAN) and in EAN adoptively transferred by P2-specific T cells (AT-EAN). The bromodeoxyuridine (BrdU) technique was employed to detect in situ proliferating cells in spleen and sciatic nerve. We assessed the nuclear morphology of infiltrating T cells using morphological criteria of apoptotic cell death. Apoptosis of lymphoid cells was also investigated using molecular labeling techniques. In AT-EAN, the number of BrdU-positive cells in splenic germinal centers peaked at day 2 after cell transfer [554 ± 267 (mean ± SEM) per mm2; controls 98 ± 35), 1 day before disease onset, and declined thereafter. BrdU incorporation in spleens from animals with active EAN peaked at day 11, around disease onset, but reached lower total values (165 ± 29 per mm2). In neither model did we observe a significant proportion of BrdU-positive T cells in the peripheral nervous system. However, T cells exhibiting morphological signs of apoptosis were detected in the sciatic nerve immediately after disease onset. The number of these cells was highest on day 7 in AT-EAN (6.6 ± 3.2 per mm2) and on day 17 in active EAN (11.2 ± 2.2 per mm2), corresponding to the maximum of T cell infiltration in both animal models. T cell activation occurs systemically and not just in the autoimmune lesion. Infiltrating T cells are eliminated by apoptosis in situ, terminating the inflammatory process. Further insight into these mechanisms may help to develop new therapeutic strategies for autoimmune disorders of the peripheral nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050437
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    Paper (German National Licenses)
    Fulltext
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