1,720,999 research outputs found
Interferon-gamma impairs phagocytosis of Escherichia coli by primary murine peritoneal macrophages stimulated with LPS and differentially modulates proinflammatory cytokine release
No full textAxonal injury, a neglected cause of CNS damage in bacterial meningitis
No full textThe contribution of axonal injury to CNS damage in bacterial meningitis was studied by histology and immunohistochemistry for amyloid-beta precursor protein in humans and experimental rabbits. Axonal injury in the white matter caused predominantly but not exclusively by ischemia was detected in all autopsy cases (n = 5) and in 11 of 15 brains of rabbits 18 to 24 hours after intracisternal infection with Streptococcus pneumoniae. This suggests a substantial contribution of axonal pathology to neurologic sequelae after bacterial meningitis
Rifampin followed by ceftriaxone for experimental meningitis decreases lipoteichoic acid concentrations in cerebrospinal fluid and reduces neuronal damage in comparison to ceftriaxone alone
No full textRifampin (RIF) releases smaller quantities of lipoteichoic acids (LTAs) from Streptococcus pneumoniae than ceftriaxone (CRO). Due to the rapid development of resistance, RIF cannot be used as a single agent for therapy of bacterial meningitis. For this reason, we compared the effect of treatment with RIF followed by treatment with CRO (RIF-CRO) or the effect of treatment with clindamycin (CLI) followed by treatment with CRO (CLI-CRO) to that of CRO alone on the concentrations of LTAs and teichoic acids in vitro. The effects of RIF-CRO on LTA concentrations in cerebrospinal fluid (CSF) and on neuronal injury were investigated in a rabbit model of S. pneumoniae meningitis. In vitro, bacterial titers were effectively reduced by CRO, RIF-CRO, and CLI-CRO when each drug was used at 10 mug/ml. The levels of release of LTAs after the initiation of therapy were lower in RIF-CRO- and CLI-CRO-treated cultures than in cultures treated with CRO alone (P < 0.05 from 3 to 12 h after initiation of treatment). Similarly, in rabbits, the increase in the amount of LTAs in CSF was lower in RIF-CRO-treated animals than in CRO-treated animals (P = 0.02). The density of dentate apoptotic granular cells was lower after RIF-CRO therapy than after CRO therapy (medians, 58.4 and 145.6/mm(2), respectively; 25th quartiles, 36.3 and 81.7/mm(2), respectively; 75th quartiles, 100.7 and 152.3/ mm(2), respectively; P = 0.03). Therefore, initiation of therapy with a protein synthesis-inhibiting antibacterial and continuation of therapy with a combination that includes a β-lactam may be a strategy to decrease neuronal injury in bacterial meningitis
Axonal injury, a neglected cause of CNS damage in bacterial meningitis
No full textThe contribution of axonal injury to CNS damage in bacterial meningitis was studied by histology and immunohistochemistry for amyloid-beta precursor protein in humans and experimental rabbits. Axonal injury in the white matter caused predominantly but not exclusively by ischemia was detected in all autopsy cases (n = 5) and in 11 of 15 brains of rabbits 18 to 24 hours after intracisternal infection with Streptococcus pneumoniae. This suggests a substantial contribution of axonal pathology to neurologic sequelae after bacterial meningitis
Neuronal apoptosis in the denate gyrus in humans with subarachnoid hemorrage and cerebral hypoxia
No full textApoptosis of dentate granule cells is a typical feature of several animal models of disease. In 20 autopsy cases of subarachnoid hemorrhage (SAH) and global cerebral hypoxia caused by protracted shock or respiratory failure, we evaluated by light microscopy and in situ tailing whether this pattern of neuronal damage also occurs in humans. In subarachnoid hemorrhage, 4.0/mm(2) (0-13.0/mm(2)) apoptotic neurons were observed in the dentate gyrus, in cerebral hypoxia 3.6/mm(2) (0-19.9/mm(2)) (p>0.05), and in 10 aged-matched control cases dying rapidly from non-neurological diseases 0/mm(2) (0-0/mm(2)) (median [range]) (p<0.001 versus SAH and hypoxia). Neuronal apoptosis in the dentate gyrus was most frequent, when death occurred later than 24 hours and less than 11 days after disease onset. Neuronal damage in the hippocampus was always necrotic. It was more severe in hypoxia than in SAH (median neuronal damage score 3 [range: 0-3] versus 0 [0-3], P<0.001). Apoptosis appears to be the predominant mechanism of death in dentate granule cells irrespective of the underlying disease, whereas neuronal death in the hippocampus generally is of necrotic morphology
Septic metastatic encephalitis: coexistence of brain damage and repair
No full textAims: Septic metastatic encephalitis (SME) arises from systemic bacterial infections and is a severe complication of sepsis with a high mortality. In this study, we examined the neuropathological findings in humans suffering from SME including white matter pathology and proliferation of neural precursor cells in the hippocampal dentate gyrus. Methods: The brains of 10 autopsy cases with SME and 10 control cases after sudden death from non-neurological causes were studied by means of immunohistochemistry. Results: We found diffuse axonal injury and demyelination in the frontal cortex (P = 0.01) as well as increased numbers of recently generatedTUC-4 expressing neurones in the hippocampal dentate gyrus in SME cases (P = 0.01). The median density of apoptotic granule cells in the dentate gyrus also was higher in SME cases, the difference, however, failed to reach statistical significance (P = 0.25). Conclusion: The coexistence of degenerative processes predominantly in the neocortex and regenerative activity in the hippocampal formation known from bacterial meningitis also characterizes the pathology of SME.Else KronerFresenius-Stiftun
Neuronal apoptosis in the denate gyrus in humans with subarachnoid hemorrage and cerebral hypoxia
No full textApoptosis of dentate granule cells is a typical feature of several animal models of disease. In 20 autopsy cases of subarachnoid hemorrhage (SAH) and global cerebral hypoxia caused by protracted shock or respiratory failure, we evaluated by light microscopy and in situ tailing whether this pattern of neuronal damage also occurs in humans. In subarachnoid hemorrhage, 4.0/mm(2) (0-13.0/mm(2)) apoptotic neurons were observed in the dentate gyrus, in cerebral hypoxia 3.6/mm(2) (0-19.9/mm(2)) (p>0.05), and in 10 aged-matched control cases dying rapidly from non-neurological diseases 0/mm(2) (0-0/mm(2)) (median [range]) (p<0.001 versus SAH and hypoxia). Neuronal apoptosis in the dentate gyrus was most frequent, when death occurred later than 24 hours and less than 11 days after disease onset. Neuronal damage in the hippocampus was always necrotic. It was more severe in hypoxia than in SAH (median neuronal damage score 3 [range: 0-3] versus 0 [0-3], P<0.001). Apoptosis appears to be the predominant mechanism of death in dentate granule cells irrespective of the underlying disease, whereas neuronal death in the hippocampus generally is of necrotic morphology
No long-term effect two years after intrauterine exposure to dexamethasone on dentate gyrus volume, neuronal proliferation and differentiation in common marmoset monkeys
No full textGlucocorticoids are prenatally administered to promote the maturation of the lungs. They, however, can affect neuronal proliferation and differentiation. In newborn marmoset monkeys, intrauterine hyperexposure to dexamethasone (DEX) resulted in a significantly decreased proliferation rate in the hippocampal dentate gyrus without affecting neuronal differentiation. In this study, marmoset monkeys received 5 mg/kg body weight DEX either during early (days 42-48) or late (days 90-96) pregnancy. The volume of the dentate granule cell layer as well as the proliferation and neuronal differentiation in the dentate gyrus of their 2-year-old offspring were investigated. The density of proliferating cells (Ki-67), apoptotic cells (in situ tailing) and cells differentiating to neurons (double cortin, TUC-4 and calretinin) were determined immunohistochemically. Analysis of the dentate granule cell layer volume showed no significant differences between early or late DEX-exposed marmosets and untreated control animals. Similarly, proliferation and neuronal differentiation in DEX-treated animals was not significantly different in comparison with controls. In summary, the decreased proliferation rate observed in newborn marmosets after intrauterine exposure to DEX was no longer detectable in their 2-year-old siblings suggesting no long-lasting effect of prenatal hyperexposure to DEX on neuronal proliferation and differentiation in the dentate gyrus of marmoset monkeys.European Commission [QLRT-2001-02758 (EUPEAH)
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