Effect of Catalase on Regional Cerebral Blood Flow and Brain Edema during the Early Phase of Experimental Pneumococcal Meningitis

Hw, Pfister; Ködel, Uwe; Dirnagl, Ulrich; Rl, Haberl; Ruckdeschel, G.; Km, Einhäupl

doi:10.1093/infdis/166.6.1442

Cited by 32 publications

(19 citation statements)

References 14 publications

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“…Roscovitine, a purine derivative References that induces apoptosis in neutrophils, is studied in mouse models. TNF-α inhibitor decrease TNF-α levels and pleocytosis in CSF 68 , blocking IL-6 intravenously in a rat model of pneumococcal meningitis reduced also pleocytosis 69 and TGF-β2 administrated intraperitoneally reduced the subarachnoid inflammation in rats with pneumococcal meningitis 54 . Intracisternal administration of the caspase-3 inhibitor reduced apoptosis in the dentate gyrus hippocampal 70 and blocking of caspase-1 demonstrated lower levels of IL-1β 71 .…”

Section: Neuronal Damage and Targets For Adjunctive Therapymentioning

confidence: 97%

“…The release of large amounts of reactive nitrogen species (RNS) and reactive oxygen species (ROS) had been documented in patient's populations, likewise, in animal model by pneumococcal meningitis and might contribute to the development of neuronal damage 52 . Treatment with superoxide dismutase mimetics and catalase (hydrogen peroxide scavenger) inhibited brain edema formation 53,54 ; antibiotic therapy prevented, in part, the oxidative stress in experimental pneumococcal meningitis 55 . Brain resident cells produce O 2 -, H 2 O 2 as part of the host immune response to invasive bacterial infection, in addition, S. pneumoniae itself is also an important source of H 2 O 2 , which is not only able to cause direct cytotoxic damage but also reacts with the host's NO to form the highly reactive species ONOO 56 .…”

Section: Nf-kbmentioning

confidence: 99%

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Pathophysiology of acute meningitis caused by Streptococcus pneumoniae and adjunctive therapy approaches

Barichello

Generoso

Collodel

et al. 2012

Arq. Neuro-Psiquiatr.

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Pneumococcal meningitis is a life-threatening disease characterized by an acute purulent infection affecting piamater, arachnoid and the subarachnoid space. The intense inflammatory host's response is potentially fatal and contributes to the neurological sequelae. Streptococcus pneumoniae colonizes the nasopharynx, followed by bacteremia, microbial invasion and blood-brain barrier traversal. S. pneumoniae is recognized by antigen-presenting cells through the binding of Toll-like receptors inducing the activation of factor nuclear kappa B or mitogen-activated protein kinase pathways and subsequent up-regulation of lymphocyte populations and expression of numerous proteins involved in inflammation and immune response. Many brain cells can produce cytokines, chemokines and others pro-inflammatory molecules in response to bacteria stimuli, as consequence, polymorphonuclear are attracted, activated and released in large amounts of superoxide anion and nitric oxide, leading to the peroxynitrite formation, generating oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage, blood-brain barrier breakdown contributing to cell injury during pneumococcal meningitis.

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Section: Neuronal Damage and Targets For Adjunctive Therapymentioning

confidence: 97%

Section: Nf-kbmentioning

confidence: 99%

Pathophysiology of acute meningitis caused by Streptococcus pneumoniae and adjunctive therapy approaches

Barichello

Generoso

Collodel

et al. 2012

Arq. Neuro-Psiquiatr.

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“…Likewise, polyethylene glycol-conjugated SOD (PEG-SOD; 10,000 U/kg iv) was effective in preventing increases in ICP and brain water content in meningitis induced by intracisternal injection of pneumococcal cell-wall components [40]. The effect of SOD infusion was more pronounced than that of catalase infusion (25,000 U/[kg· h] iv) in the same model [48]. Perhaps more important, SOD reduced ICP and brain water content when given as late as 3 hours after intracerebral inoculation of pneumococci.…”

Section: Molecular Mechanisms Of Neuronal Injurymentioning

confidence: 99%

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Pfister

Fontana²,

Täuber³

et al. 1994

Clinical Infectious Diseases

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Morbidity and mortality associated with bacterial meningitis remain high, although antibiotic therapy has improved during recent decades. The major intracranial complications of bacterial meningitis are cerebrovascular arterial and venous involvement, brain edema, and hydrocephalus with a subsequent increase of intracranial pressure. Experiments in animal models and cell culture systems have focused on the pathogenesis and pathophysiology of bacterial meningitis in an attempt to identify the bacterial and/or host factors responsible for brain injury during the course of infection. An international workshop entitled "Bacterial Meningitis: Mechanisms of Brain Injury" was organized by the Department of Neurology at the University of Munich and was held in Eibsee, Germany, in June 1993. This conference provided a forum for the exchange of current information on bacterial meningitis, including data on the clinical spectrum of complications, the associated morphological alterations, the role of soluble inflammatory mediators (in particular cytokines) and of leukocyte-endothelial cell interactions in tissue injury, and the molecular mechanisms of neuronal injury, with potential mediators such as reactive oxygen species, reactive nitrogen species, and excitatory amino acids. It is hoped that a better understanding of the pathophysiological events that take place during bacterial meningitis will lead to the development of new therapeutic regimens.Although the recent licensure of Haeniophilus influenzae type b (Hib) polysaccharide conjugate protein vaccines has had a marked impact on the incidence of invasive Hib disease in the United States and Western Europe. bacterial meningitis overall remains a significant problem worldwide. In addition, despite the introduction of new antimicrobial agents and improved diagnostic techniques, the mortality and morbidity associated with bacterial meningitis remain unacceptably high. This discrepancy between a rapid bacteriologic response at the site of infection (i.e .. eradication of viable bacteria from the CSF due to treatment with potent bactericidal agents) and the persistence of the associated neurological sequelae and mortality has prompted intense investigation over the past two decades into the pathophysiology of this disease. Indeed. recent clinical studies have employed adjunctive agents (e.g .. dexamethasone) in an attempt to reduce mortality and alleviate neurological sequelae [1][2][3][4]. These studies and the resulting recommendations regarding the use of adjunctive dexamethasone have recently been reviewed [5.6].In line with the current emphasis on the pathogenesis and pathophysiology of bacterial meningitis. two workshops were held in California in the 1980s [7]. Recognizing that many advances have been made in this field in the several years since those meetings. the Department of Neurology at the University of Munich organized a similar workshop, which was held in Eibsce. Germanv. on 25 and 26 June 1993. As IS evident from its title-"Bacterial Meningitis: Mechanisms...

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“…Experimental and endogenous antioxidants (␣-phenyl-tertbutyl, superoxide dismutase, catalase, the 21-aminosteroid U74389F, and uric acid) (54,73,81,83,116,117,119) and several clinically used antioxidants (N-acetylcysteine, desferoxamine, and trylizad mesylate) (8) reduce brain edema, cortical damage, and changes in cerebral blood flow in experimental meningitis. Assessment of the effect on hippocampal neurons produced conflicting results, varying from reduction of apoptosis by ␣-phenyl-tert-butyl in group B streptococcal meningitis to aggravated apoptosis and learning deficits with the same agent in pneumococcal meningitis (73,81).…”

Section: Conserve Cellular Function (I) Blood-brain Barrier and Incrmentioning

confidence: 99%

Reprogramming the Host Response in Bacterial Meningitis: How Best To Improve Outcome?

et al. 2003

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Despite effective antibiotic therapy, bacterial meningitis is still associated with high morbidity and mortality in both children and adults. Animal studies have shown that the host inflammatory response induced by bacterial products in the subarachnoid space is associated with central nervous system injury. Thus, attenuation of inflammation early in the disease process might improve the outcome. The feasibility of such an approach is demonstrated by the reduction in neurologic sequelae achieved with adjuvant dexamethasone therapy. Increased understanding of the pathways of inflammation and neuronal damage has suggested rational new targets to modulate the host response in bacterial meningitis, but prediction of which agents would be optimal has been difficult. This review compares the future promise of benefit from the use of diverse adjuvant agents. It appears unlikely that inhibition of a single proinflammatory mediator will prove useful in clinical practice, but several avenues to reprogram a wider array of mediators simultaneously are encouraging. Particularly promising are efforts to adjust combinations of cytokines, to inhibit neuronal apoptosis and to enhance brain repair

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Effect of Catalase on Regional Cerebral Blood Flow and Brain Edema during the Early Phase of Experimental Pneumococcal Meningitis

Cited by 32 publications

References 14 publications

Pathophysiology of acute meningitis caused by Streptococcus pneumoniae and adjunctive therapy approaches

Pathophysiology of acute meningitis caused by Streptococcus pneumoniae and adjunctive therapy approaches

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Reprogramming the Host Response in Bacterial Meningitis: How Best To Improve Outcome?

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