Soluble intercellular adhesion molecule-1 in cerebrospinal fluid: An indicator for the inflammatory impairment of the blood-cerebrospinal fluid barrier

Rieckmann, Peter; Nünke, K.; Burchhardt, M.; Albrecht, M.; Wiltfang, Jens; Ulrich, Michael; Felgenhauer, K.

doi:10.1016/0165-5728(93)90023-r

Cited by 89 publications

(38 citation statements)

References 33 publications

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“…For details see [167] ▸ allowing them to resist the shear forces exerted by the CSF flow. In addition, apical ICAM-1 and VCAM-1 may be the source for soluble ICAM-1 and VCAM-1 found in increased concentrations in the CSF of patients with multiple sclerosis, viral encephalitis or bacterial meningitis [118,125].…”

Section: Neuroimmune Function Of the Choroid Plexuses In Neurologicalmentioning

confidence: 99%

Molecular anatomy and functions of the choroidal blood-cerebrospinal fluid barrier in health and disease

et al. 2018

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The barrier between the blood and the ventricular cerebrospinal fluid (CSF) is located at the choroid plexuses. At the interface between two circulating fluids, these richly vascularized veil-like structures display a peculiar morphology explained by their developmental origin, and fulfill several functions essential for CNS homeostasis. They form a neuroprotective barrier preventing the accumulation of noxious compounds into the CSF and brain, and secrete CSF, which participates in the maintenance of a stable CNS internal environment. The CSF circulation plays an important role in volume transmission within the developing and adult brain, and CSF compartments are key to the immune surveillance of the CNS. In these contexts, the choroid plexuses are an important source of biologically active molecules involved in brain development, stem cell proliferation and differentiation, and brain repair. By sensing both physiological changes in brain homeostasis and peripheral or central insults such as inflammation, they also act as sentinels for the CNS. Finally, their role in the control of immune cell traffic between the blood and the CSF confers on the choroid plexuses a function in neuroimmune regulation and implicates them in neuroinflammation. The choroid plexuses, therefore, deserve more attention while investigating the pathophysiology of CNS diseases and related comorbidities.

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Section: Neuroimmune Function Of the Choroid Plexuses In Neurologicalmentioning

confidence: 99%

Molecular anatomy and functions of the choroidal blood-cerebrospinal fluid barrier in health and disease

et al. 2018

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“…Increased expression of ICAM-1 is observed in inflammatory processes, it promotes the influx of peripheral immune cells through the BBB. 122 By this mechanism, macrophages and co-stimulatory lymphocytes can invade the CNS, further increasing the proinflammatory immune response. Inflammation is associated with increased invasion of macrophages/ microglia in the CNS.…”

Section: The Inflammatory Hypothesis Of Depressionmentioning

confidence: 99%

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

2007

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Beside the well-known deficiency in serotonergic neurotransmission as pathophysiological correlate of major depression (MD), recent evidence points to a pivotal role of increased glutamate receptor activation as well. However, cause and interaction of these neurotransmitter alterations are not understood. In this review, we present a hypothesis integrating current concepts of neurotransmission and hypothalamus-pituitary-adrenal (HPA) axis dysregulation with findings on immunological alterations and alterations in brain morphology in MD. An immune activation including increased production of proinflammatory cytokines has repeatedly been described in MD. Proinflammatory cytokines such as interleukin-2, interferon-c, or tumor necrosis factor-a activate the tryptophan-and serotonin-degrading enzyme indoleamine 2,3-dioxygenase (IDO). Depressive states during inflammatory somatic disorders are also associated with increased proinflammatory cytokines and increased consumption of tryptophan via activation of IDO. An enhanced consumption of serotonin and its precursor tryptophan through IDO activation could well explain the reduced availability of serotonergic neurotransmission in MD. An increased activation of IDO and its subsequent enzyme kynurenine monooxygenase by proinflammatory cytokines, moreover, leads to an enhanced production of quinolinic acid, a strong agonist of the glutamatergic N-methyl-D-aspartate receptor. In inflammatory states of the central nervous system, IDO is mainly activated in microglial cells, which preferentially metabolize tryptophan to the NMDA receptor agonist quinolinic acid, whereas astrocytes -counteracting this metabolism due to the lack of an enzyme of this metabolism -have been observed to be reduced in MD. Therefore the type 1/type 2 immune response imbalance, associated with an astrocyte/microglia imbalance, leads to serotonergic deficiency and glutamatergic overproduction. Astrocytes are further strongly involved in re-uptake and metabolic conversion of glutamate. The reduced number of astrocytes could contribute to both, a diminished counterregulation of IDO activity in microglia and an altered glutamatergic neurotransmission. Further search for antidepressant agents should take into account anti-inflammatory drugs, for example, cyclooxygenase-2 inhibitors, might exert antidepressant effects by acting on serotonergic deficiency, glutamatergic hyperfunction and antagonizing neurotoxic effects of quinolinic acid. Molecular Psychiatry (2007) 12, 988-1000; doi:10.1038/sj.mp.4002006; published online 24 April 2007 Keywords: major depression; psychoneuroimmunology; IDO; glutamate; immune system; serotonin Glutamate in depressionGlutamatergic neurotransmission is involved in depression and interacts with the serotonergic and noradrenergic systems The common therapeutic mechanism of antidepressant drugs is the enhancement of serotonergic and/or noradrenergic neurotransmission. On the basis of this pharmacological profile of antidepressant drugs, neurochemical research on major depression ...

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“…Adhesion molecules play an important role in the migration of immune cells into the CNS. Patients with MS have increased serum levels of soluble ICAM-1 (sICAM-1), 36,37 and recent studies 9,38 have shown that ICAM-1 is more important than other adhesion molecules in promoting pathological cell infiltration into the CNS and the development of EAE. To determine whether this molecule is involved in the EGCGinduced reduction of inflammatory infiltration, we measured the plasma sICAM-1 level and found that it was lower in mice fed EGCG compared with those fed the control diet ( Figure 9A).…”

Section: Egcg Reduces Circulating Icam-1 and Downregulates Ccr6 Exprementioning

confidence: 99%

Epigallocatechin-3-Gallate Ameliorates Experimental Autoimmune Encephalomyelitis by Altering Balance among CD4+ T-Cell Subsets

Wang

Ren

et al. 2012

The American Journal of Pathology

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The green tea component epigallocatechin-3-gallate (EGCG) may be beneficial in autoimmune diseases; however, the underlying mechanisms are not well understood. In this study, we determined the effect of EGCG on the development of experimental autoimmune encephalomyelitis, an animal model for human multiple sclerosis, and the underlying mechanisms. Female C57BL/6 mice were fed EGCG (0%, 0.15%, 0.3%, and 0.6% in diet) for 30 days and then immunized with specific antigen myelin oligodendrocyte glycoprotein 35-55. EGCG dose dependently attenuated clinical symptoms and pathological features (leukocyte infiltration and demyelination) in the central nervous system and inhibited antigen-specific T-cell proliferation and delayed-type hypersensitivity skin response. We further showed that EGCG reduced production of interferon-␥, IL-17, IL-6, IL-1␤, and tumor necrosis factor-␣; decreased types 1 and 17 helper T cells (Th1 and Th17, respectively); and increased regulatory T-cell populations in lymph nodes, the spleen, and the central nervous system. Moreover, EGCG inhibited expression of transcription factors T-box expressed in T cells and retinoid-related orphan receptor-␥t, the specific transcription factor for Th1 and Th17 differentiation, respectively; the plasma levels of intercellular adhesion molecule 1; and CCR6 expression in CD4 ؉ T cells. These results indicate that EGCG may attenuate experimental autoimmune encephalomyelitis autoimmune response by inhibiting immune cell infiltration and modulating the balance among pro-and anti-autoimmune CD4 ؉ T-cell subsets.Thus, we identified a novel mechanism that underlies EGCG's beneficial effect in autoimmune disease. (Am J

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Soluble intercellular adhesion molecule-1 in cerebrospinal fluid: An indicator for the inflammatory impairment of the blood-cerebrospinal fluid barrier

Cited by 89 publications

References 33 publications

Molecular anatomy and functions of the choroidal blood-cerebrospinal fluid barrier in health and disease

Molecular anatomy and functions of the choroidal blood-cerebrospinal fluid barrier in health and disease

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

Epigallocatechin-3-Gallate Ameliorates Experimental Autoimmune Encephalomyelitis by Altering Balance among CD4+ T-Cell Subsets

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