Production and function of monocyte chemoattractant protein-1 and other β-chemokines in murine glial cells

Hayashi, Masaharu; Luo, Yi; Laning, Joseph; Strieter, Robert M.; Dorf, Martin E.

doi:10.1016/0165-5728(95)00064-9

Cited by 220 publications

(144 citation statements)

References 44 publications

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“…30,[45][46][47][48][49] Luo and colleagues 50 have previously reported that astrocyte production of CCL2 in response to RANTES is TNF-dependent. Therefore the reduction in early CCL2 production in TNFR1-null hosts could result from an astrocyte deficiency in TNFR1.…”

Section: Discussionmentioning

confidence: 99%

A Tumor Necrosis Factor Receptor 1-Dependent Conversation between Central Nervous System-Specific T Cells and the Central Nervous System Is Required for Inflammatory Infiltration of the Spinal Cord

Gimenez

Sim

Archambault

et al. 2006

The American Journal of Pathology

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Experimental autoimmune encephalomyelitis (EAE) is an autoimmune demyelinating disease of the central nervous system (CNS). Because of similarities in clinical symptoms and CNS histology, 1-5 EAE serves as a model for multiple sclerosis and can be induced in mice by either immunization with myelin protein or peptides 6 or by adoptive transfer of myelin-specific Th1 CD4 ϩ T cells. 7,8As a result, inflammatory cells consisting mostly of CD4 ϩ T lymphocytes and macrophages infiltrate the CNS leading to demyelination and neuronal damage. 9Tumor necrosis factor receptor 1 (TNFR1), also known as the p55 kd TNF receptor, binds to two ligands, TNF and lymphotoxin-␣. 10 The dominant signaling pathway for TNFR1 promotes inflammation by up-regulating inflammatory cytokines, chemokines, and adhesion molecules 11-17 and also suppresses apoptosis by the induction of IAPs (inhibitors of apoptosis) through nuclear factor (NF)-B-dependent pathways.18 TNFR1 also has the ability to induce apoptosis through a death domain in its cytoplasmic region that initiates the FADD-dependent extrinsic apoptotic pathway. 19Our previous experiments have demonstrated that TNFR1 contributes to the pathogenesis of EAE mainly by promoting CNS inflammation, 20 and thereby, in the absence of TNFR1 expression, clinical disease is limited. Through our adoptive transfer experiments we have found a dramatic difference in the location of encephalitogenic T cells within the CNS of wild-type (WT) versus TNFR1-null mice. Although we observed equivalent numbers of T cells in the CNS of TNFR1-deficient mice compared to WT mice, we found that the T cells in the TNFR1-null animals were confined to the leptomeninges and perivascular spaces of the spinal cord, whereas in the

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Section: Discussionmentioning

confidence: 99%

A Tumor Necrosis Factor Receptor 1-Dependent Conversation between Central Nervous System-Specific T Cells and the Central Nervous System Is Required for Inflammatory Infiltration of the Spinal Cord

Gimenez

Sim

Archambault

et al. 2006

The American Journal of Pathology

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“…A subpopulation of astroglia express functional MOR (Eriksson et al, 1991;Stiene-Martin and Hauser, 1991;Hauser et al, 1996;Stiene-Martin et al, 1998;Stiene-Martin et al, 2001) and opiates markedly increase the production of chemokines by HIV-1 Tat exposed astrocytes . Astrocytes are an important source of chemokines in the CNS and express CCL2 (Ransohoff et al, 1993;Hayashi et al, 1995;Peterson et al, 1997;Oh et al, 1999) and variably express its cognate receptor CCR2 (Andjelkovic et al, 1999;Dorf et al, 2000), although CCR2 expression among astrocytes is heterogeneous and appears to be regulated by inflammation (Andjelkovic et al, 2002;Croitoru-Lamoury et al, 2003). HIV-1 Tat triggers CCL2 production and inflammatory cascades in astrocytes (Conant et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

CCR2 mediates increases in glial activation caused by exposure to HIV-1 Tat and opiates

El‐Hage

Ambati

et al. 2006

Journal of Neuroimmunology

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To assess the role of CCL2/MCP-1 in opiate drug abuse and HIV-1 comorbidity, the effects of systemic morphine and intrastriatal HIV-1 Tat on macrophage/microglial and astroglial activation were assessed in wild type and CCR2 null mice. Tat and/or morphine additively increased the proportion of CCL2 immunoreactive astroglia. The effects of morphine were prevented by naltrexone. Glial activation was significantly reduced in CCR2(−/−) versus wild-type mice following Tat or morphine plus Tat exposure. Thus, CCR2 contributes to local glial activation caused by Tat alone or in the presence of opiates, implicating CCR2 signaling in HIV-1 neuropathogenesis in drug abusers and non-abusers.

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“…Additionally, stimulated astrocytes can express MIP-1a and MIP-1b and RANTES (Barnes et al, 1996). LPS, IL-1b and TNF-a stimulate production of MCP-1 by astrocytes but not microglia (Hayashi et al, 1995). HIV-1 transactivator protein Tat signi®cantly increase astrocyte production of MCP-1, but not RANTES, MIP-1a and MIP-1b suggesting that HIV may induce monocyte in®ltration in the CNS via astrocyte stimulation (Conant et al, 1998).…”

Section: Chemokine Expression By Cns Cells In Vitromentioning

confidence: 99%

“…Ehrlich et al, 1998;Lipovsky et al, 1998;Lokensgard et al, 1997;Sopper et al, 1996;Sun et al, 1997;Hurwitz et al, 1995;Fisher et al, 1995;Hayashi et al, 1995;Meda et al, 1996;Calvo et al, 1996 MCP-1, IL-8 Stimulated cerebral endothelium Human, bovine, porcine, murine …”

Section: Chemokine Receptors In Cns Pathologymentioning

confidence: 99%

Chemokines and chemokine receptors in CNS pathology

Głąbiński¹,

Ransohoff²

1999

J Neurovirol

168

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Production and function of monocyte chemoattractant protein-1 and other β-chemokines in murine glial cells

Cited by 220 publications

References 44 publications

A Tumor Necrosis Factor Receptor 1-Dependent Conversation between Central Nervous System-Specific T Cells and the Central Nervous System Is Required for Inflammatory Infiltration of the Spinal Cord

A Tumor Necrosis Factor Receptor 1-Dependent Conversation between Central Nervous System-Specific T Cells and the Central Nervous System Is Required for Inflammatory Infiltration of the Spinal Cord

CCR2 mediates increases in glial activation caused by exposure to HIV-1 Tat and opiates

Chemokines and chemokine receptors in CNS pathology

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