Journal of neuroimmunology
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In the present study, intraperitoneal administration of minocycline attenuated enhancing nociceptive behaviors in those rats receiving dual formalin injections (5% formalin followed at 7 days later by 1% formalin). The minocycline treatment did not prevent the increase in OX-42 and MHC class I labeling and morphological changes, but significantly attenuated upregulation of phospho-p38 in activated microglia. These results suggest that the later days of microglial activation with upregulated immune markers in the spinal cord contributes to enhancing long-term pain response by a pathway of p38 activation in microglia.
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Bacterial meningitis caused by Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae, including sensory-motor deficits, seizures, and impairment of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response at killing the invading microorganism. Proinflammatory mediators released in the process, including tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, were shown to contribute to the development of brain injury in bacterial meningitis. ⋯ In the hippocampus we found increased levels of the TNF-alpha only at 6h (p<0.01; F=3.777); CINC-1 levels increased at 6 and 24h (p<0.001; p<0.05; F=15.05); and IL-6 and IL-1beta levels were not altered. In the prefrontal cortex, the TNF-alpha levels were found to be increased only at 6h (p<0.05; F=4.921); IL-6 (p<0.05; F=11.69) and IL-1beta (p<0.001; F=132.0) levels were found to be increased only at 24h after meningitis induction; and CINC-1 levels were found to be increased at 6, 12, and 24h (p<0.01; p<0.01; p<0.01; F=16.86) after meningitis induction. Our data suggest that cytokine/chemokine levels can be putative biomarkers of brain damage in the first hours of the pneumococcal meningitis.
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Calprotectin is produced by activated monocytes and microglia, and cerebrospinal fluid (CSF) levels could be a marker of neuroinflammation. Calprotectin was detectable in CSF from 13.8% of normal controls, compared to 90.5% of patients with neurological infections (p<0.001). In CSF from patients with multiple sclerosis (MS) and clinically isolated demyelinating syndrome, calprotectin was detected in 64.7% within 2 weeks after symptom debut compared to 30.8% between 2 and 4 weeks and 17.0% thereafter (p<0.001). We conclude that CSF calprotectin reflects the disease activity in MS but does not discriminate between MS and other inflammatory or infectious conditions.
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Since identification of the autoantibodies in Fisher syndrome, remarkable progress has been made in our understanding of that syndrome and related conditions. Because of the similarities in the clinical presentations of it and Bickerstaff brainstem encephalitis, opinions differ as to whether the two are distinct or related syndromes and whether the lesions responsible for ophthalmoplegia, ataxia and areflexia are in the peripheral or central nervous system. The finding that both conditions have autoantibodies in common suggested that the autoimmune mechanism is the same in both and they are not distinct conditions. ⋯ A new eponymic terminology "Fisher-Bickerstaff syndrome" may be helpful for nosology. A considerable number of patients with Bickerstaff brainstem encephalitis have associated Guillain-Barré syndrome, indicative that these two disorders are closely related on a continuous spectrum. That finding is further evidence of continuity between Bickerstaff brainstem encephalitis and Fisher syndrome, a variant of Guillain-Barré syndrome.
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Clinical Trial
Effects of vagus nerve stimulation on pro- and anti-inflammatory cytokine induction in patients with refractory epilepsy.
The role of the vagus nerve in controlling and modulating inflammatory responses under physiological conditions has been investigated. The purpose of this study is to assess changes in the immunological state evoked by vagus nerve stimulation in humans, by measuring cytokines produced by peripheral blood mononuclear cells (PBMC). ⋯ No significant changes were seen in the induction of IL-1beta, TNF-alpha, IL-6 or IL-10. The present study shows that cytokine induction by PBMC isolated from patients with refractory epilepsy is altered by long-term vagus nerve stimulation.