Immunocompetence of human microvascular brain endothelial cells: cytokine regulation of IL-1β, MCP-1, IL-10, sICAM-1 and sVCAM-1

Frigerio, Simona; Gelati, Maurizio; Ciusani, Emilio; Corsini, E.; Dufour, A.; Massa, G; Salmaggi, Andrea

doi:10.1007/s004150050275

Cited by 34 publications

(29 citation statements)

References 16 publications

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“…One group recently reported that brain cell injury from B. burgdorferi is not directly caused by the Lyme disease spirochete or its lipoproteins but by microglia (44). Others have reported that endothelial cells do not produce IL-10 in response to exposure to B. burgdorferi (56), TNF, IFN-g, or LPS (57). An important protective role of IL-10 for the cerebral microcirculation has been shown in several systemic infections (58), including cerebral malaria (59,60) and African trypanosomiasis (61).…”

Section: Discussionmentioning

confidence: 99%

IL-10 Prevents Apoptosis of Brain Endothelium during Bacteremia

Londoño

Carvajal

Strle

et al. 2011

The Journal of Immunology

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IL‐10 deficient mice infected with the relapsing fever bacterium Borrelia turicatae rapidly succumb to brain hemorrhage if they are unable to clear peak bacteremia. Here we investigated the protective role of IL‐10 during relapsing‐remitting bacterial infection and explored the molecular events involved in protection of brain endothelium by IL‐10. The results showed that severe endothelial cell injury leading to hemorrhage in the brain and other organs occurred in IL‐10 deficient mice during relapsing‐remitting infection. Human brain microvascular endothelial cells (HBMEC) upon exposure to whole bacteria or purified bacterial lipoprotein are rapidly killed by apoptosis and produced abundant pro‐inflammatory mediators but did not produce any IL‐10. HBMEC apoptosis during exposure to low number of bacteria was associated with down regulation of TNF and TNFAIP3 and upregulation of BAX. In contrast, exposure to high concentrations of purified outer membrane lipoprotein was associated with dramatic upregulation of FAS, FAS ligand, and the adaptor molecules RIPK1 and CFLAR. Exogenous IL‐10 reversed all the apoptotic signaling changes induced by whole bacteria or purified lipoprotein. The results indicate that IL‐10 prevent brain endothelial cell injury and point to a prominent role for bacterial lipoprotein mediated activation of different apoptosis pathways in this process.

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Section: Discussionmentioning

confidence: 99%

IL-10 Prevents Apoptosis of Brain Endothelium during Bacteremia

Londoño

Carvajal

Strle

et al. 2011

The Journal of Immunology

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“…Human brain microvascular endothelial cells (HBMEC) were obtained from microvessels included in the apparently normal white matter of surgical specimens of a patient affected from MS and operated on because of a right middle cerebral artery aneurysm. (16) After removal of leptomeninges and vessels from the surgical specimen, HBMEC were isolated by trypsinization, filtration through a 100-mesh screen, and centrifugation in 15% dextran. (17) The cells were incubated in collagenase and plated on collagen-coated dishes.…”

Section: Methodsmentioning

confidence: 99%

In Vitro Modulation of Adhesion Molecules, Adhesion Phenomena, and Fluid Phase Endocytosis on Human Umbilical Vein Endothelial Cells and Brain-Derived Microvascular Endothelium by IFN-β1a

Defazio

Gelati

Corsini

et al. 2001

Journal of Interferon & Cytokine Research

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Administration of interferon-beta (IFN-beta) in multiple sclerosis (MS) patients provides clinical benefits, although its mechanism(s) of action are not completely understood. We addressed the issue of whether concentrations of IFN-beta1a close to those reached in the serum of treated MS patients could modulate either adhesion molecules or adhesion of peripheral blood mononuclear cells (PBMC) as well as fluid phase endocytosis (FPE) in human umbilical vein endothelial cells (HUVEC) and in brain-derived microvascular endothelial cells (HBMEC). Adhesion was assessed by flow cytometry, and FPE was evaluated by peroxidase uptake. In our study, 200 U/ml IFN-beta1a induced a reduction in adhesion of PBMC to HUVEC. The information reported herein may contribute to further elucidating some of the mechanisms of action of IFN-beta on vascular endothelium.

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“…In addition to expression of adhesion molecules, BMEC can produce a spectrum of inflammatory cytokines, including interleukin (IL)-1 β (Frigerio et al, 1998), IL-6 , and tumor necrosis factor-α (TNF-α) (Botchkina et al, 1997) as well as chemokines, such as monocyte chemoattractant protein-1 (MCP-1) (Zhang et al, 1999) and IL-8/CXCL8 .…”

Section: Hiv-1 Entry Into the Cns: The Role Of Brain Endothelial Cellmentioning

confidence: 99%

Mechanisms of the Blood–Brain Barrier Disruption in HIV-1 Infection

et al. 2005

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(1) Alterations of brain microvasculature and the disruption of the blood-brain barrier (BBB) integrity are commonly associated with human immunodeficiency virus type 1 (HIV-1) infection. These changes are most frequently found in human immunodeficiency virus-related encephalitis (HIVE) and in human immunodeficiency virus-associated dementia (HAD). (2) It has been hypothesized that the disruption of the BBB occurs early in the course of HIV-1 infection and can be responsible for HIV-1 entry into the CNS. (3) The current review discusses the mechanisms of injury to brain endothelial cells and alterations of the BBB integrity in HIV-infection with focus on the vascular effects of HIV Tat protein. In addition, this review describes the mechanisms of the BBB disruption due to HIV-1 or Tat protein interaction with selected risk factors for HIV infection, such as substance abuse and aging.

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Immunocompetence of human microvascular brain endothelial cells: cytokine regulation of IL-1β, MCP-1, IL-10, sICAM-1 and sVCAM-1

Cited by 34 publications

References 16 publications

IL-10 Prevents Apoptosis of Brain Endothelium during Bacteremia

IL-10 Prevents Apoptosis of Brain Endothelium during Bacteremia

In Vitro Modulation of Adhesion Molecules, Adhesion Phenomena, and Fluid Phase Endocytosis on Human Umbilical Vein Endothelial Cells and Brain-Derived Microvascular Endothelium by IFN-β1a

Mechanisms of the Blood–Brain Barrier Disruption in HIV-1 Infection

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