Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A soluble form of the intercellular adhesion molecule-1 (sICAM-1) was measured in paired cerebrospinal fluid (CSF)/blood samples from 123 patients with different neurological diseases. Mean levels of circulating ICAM-1 in the blood were mean +/- SD = 423 +/- 184.6 ng ml-1 (range 44-1115 ng ml-1). Considerable differences of sICAM-1 in the CSF of patients were observed between disease groups. In acute bacterial meningitis, sICAM-1 levels as high as 1/5 of the serum concentration were detected in the CSF (n = 24; mean +/- SD = 33.0 +/- 23.7 ng ml-1; range: 4.8-93.9 ng ml-1). These changes coincided with a severe blood-CSF barrier dysfunction as indicated by a high CSF/blood ratio for albumin (mean +/- SD = 46.7 +/- 52.2; range: 16.8-249.3). In patients with polyradiculitis (n = 9; mean +/- SD = 14.5 +/- 11.9 ng ml-1; range: 2.6-43.7 ng ml-1) a similar covariation between the albumin and sICAM CSF/blood ratios was detected. In patients with multiple sclerosis (n = 9; mean +/- SD = 5 +/- 4.3; range: 0-12.7 ng ml-1) or HIV infection with neurological symptoms (n = 18; mean +/- SD = 4.9 +/- 3.2; range; 1-11.9 ng ml-1) low levels of sICAM-1 were detected in the CSF associated with intact blood-CSF barrier function in most patients. Among 13 patients with viral meningitis, only four had detectable levels of sICAM-1 in their CSF (mean +/- SD = 1.0 +/- 1.5 ng ml-1; range: 0-3.7).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Soluble intercellular adhesion molecule-1 in cerebrospinal fluid: an indicator for the inflammatory impairment of the blood-cerebrospinal fluid barrier. 810 75

We measured soluble intercellular adhesion molecule-1 (sICAM-1) in the serum and cerebrospinal fluid (CSF) of 35 clinically active relapsing-remitting (RR) multiple sclerosis (MS) patients who underwent both lumbar puncture and gadopentetate dimeglumine (Gd-DTPA)-enhanced MRI within an interval of 1 week, and of 30 neurological controls of whom 17 had noninflammatory neurologic diseases (NIND), 8 bacterial meningitis (BM), and 5 AIDS dementia complex (ADC). Thirteen of the MS patients assumed corticosteroids at the time of the study. While sICAM-1 serum levels were highest in the BM group (p < 0.005), untreated MS patients showed levels higher (p < 0.05) than treated MS and NIND, but similar to ADC. Moreover, the untreated MS group had CSF/serum sICAM-1:CSF/serum albumin (sICAM-1 index) values higher than the treated group (p < 0.01), NIND (p < 0.005), and BM (p < 0.05); high sICAM-1 index was found also in ADC. Untreated MS patients with one or more Gd-DTPA-enhancing MRI lesions (Gd-positive) had higher mean values of CSF/serum albumin ratio (QAlbumin) and CSF mononuclear cells compared to patients without such lesions (Gd-negative). In the untreated Gd-negative patients, sICAM-1 serum levels were higher (p < 0.05) than those in Gd-positive patients. In the latter group, there were positive correlations between the number of CSF mononuclear cells and both IgG (p < 0.01) and sICAM-1 indices (p < 0.05), between QAlbumin and QsICAM-1 (p < 0.005) and between Qalbumin and the Expanded Disability Status Scale score (p = 0.05). There were no significant correlations in the Gd-negative group. These results suggest that sICAM-1 index can be a better marker of intrathecal sICAM-1 synthesis than CSF levels and provide additional insights, in vivo, into the blood-brain barrier mechanisms underlying MRI Gd-enhancement in clinically active RR MS.
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PMID:Soluble intercellular adhesion molecule-1 in serum and cerebrospinal fluid of clinically active relapsing-remitting multiple sclerosis: correlation with Gd-DTPA magnetic resonance imaging-enhancement and cerebrospinal fluid findings. 896 Jul 41

The soluble intercellular adhesion molecule-1 (sICAM-1) was measured in paired CSF and serum samples from 128 patients with different neurological diseases. The reference range of blood-derived sICAM-1 fractions in CSF was characterized with reference to the albumin CSF/serum quotients. The low mean concentrations of sICAM-1 of normal controls (n=33) in CSF (1.5 ng/ml; C.V.=40%) compared to serum (285.1 ng/ml; C.V.=32%) indicate that about 60% to 80% of sICAM-1 in normal lumbar CSF derives from blood. This calculation is based on the theoretically expected molecular size-dependent blood-CSF gradient between 300:1 to 250:1. In patients with non-inflammatory diseases (n=21) the sICAM-1 CSF/serum quotient increased non-linearly with increasing albumin CSF/serum quotient (blood-CSF barrier dysfunction) displaying the shape of a saturation-like curve in contrast to hyperbolic curves of other blood-derived proteins in CSF. This non-linear relation between sICAM-1 and albumin quotients does not allow a linear index evaluation reported in earlier studies. In bacterial meningitis (n=31) and viral meningoencephalitis (n=28) in addition to the increased blood-derived fraction, the brain-derived fraction of sICAM-1 in CSF was up to 12-fold higher than that in controls. The sICAM-1 CSF/serum quotients in MS (n=15) did not differ from non-inflammatory controls, i.e., there was no brain-dependent sICAM-1 fluctuation in CSF in contrast to the known fluctuations in blood. Earlier published reports on sICAM-1 have been controversial due to less sensitive assays and unsuitable linear evaluation concepts for blood-CSF barrier dysfunction.
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PMID:Intercellular adhesion molecule-1 in cerebrospinal fluid--the evaluation of blood-derived and brain-derived fractions in neurological diseases. 967 Aug 57

Leukocyte-endothelial adhesion molecules, critical to the development of acute inflammation, are expressed in brain as part of the acute inflammatory response to traumatic brain injury (TBI). We measured the concentrations of the adhesion molecules P-selectin, ICAM-1, E-selectin, L-selectin, and VCAM-1 in ventricular cerebrospinal fluid (CSF) from children with severe TBI (Glasgow coma score < 8) and compared these findings with those from children with bacterial meningitis. P-selectin, an adhesion molecule associated with ischemia/reperfusion, was increased in children with TBI versus meningitis and control. Univariate and multivariate regression analyses demonstrated associations between CSF P-selectin and child abuse and age of < 4 years, and a significant, independent association between CSF intercellular adhesion molecule-1 (ICAM-1) and child abuse. These results are consistent with a specific acute inflammatory component to TBI in children. Future studies of secondary injury mechanisms and therapy after TBI should assess on the roles of P-selectin and ICAM-1 in injury and repair processes in brain after TBI.
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PMID:Soluble adhesion molecules in CSF are increased in children with severe head injury. 981 34

Nitric oxide (NO) plays a central role in the pathogenesis of bacterial meningitis. However, the role of NO produced by endothelial NO synthase (eNOS) in meningitis is still unclear. We investigated the influence of eNOS depletion on the inflammatory host response, intracranial complications, and outcome in experimental pneumococcal meningitis. Leukocyte accumulation in the cerebrospinal fluid was more pronounced in infected eNOS-deficient mice than in infected wild type mice. This effect could be attributed to an increased expression of P-selectin, macrophage inflammatory protein-2, keratinocyte-derived cytokine, and interleukin (IL)-1beta in the brain of infected eNOS-deficient mice. However, no differences in the cerebral expression of intercellular adhesion molecule-1, tumor necrosis factor-alpha, and IL-6 as well as of neuronal NOS and inducible NOS could be detected between infected wild type and mutant mice. In addition to enhanced leukocyte infiltration into the CSF, meningitis-associated intracranial complications including blood-brain barrier disruption and the rise in intracranial pressure were significantly augmented in infected eNOS-deficient mice. The aggravation of intracranial complications was paralleled by a worsening of the disease, as evidenced by a more pronounced hypothermia, an enhanced weight reduction, and an increased death rate. The current data indicate that eNOS deficiency is detrimental in bacterial meningitis. This effect seems to be related to an increased expression of (certain) cytokines/chemokines and adhesion molecules; thus leading to increased meningeal inflammation and, subsequently, to aggravated intracranial complications.
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PMID:Lack of endothelial nitric oxide synthase aggravates murine pneumococcal meningitis. 1170 34