Synergistic stimulation, by tumor necrosis factor-α and interferon-γ, of fractalkine expression in human astrocytes

Yoshida, Hidemi; Imaizumi, Tadaatsu; Fujimoto, Koji; Matsuo, Naomi; Kimura, Kazuyuki; Cui, Xuefan; Matsumiya, Tomoh; Tanji, Kunikazu; Shibata, Takeo; Tamo, Wakako; Kumagai, Mika; Satoh, Kei

doi:10.1016/s0304-3940(01)01699-8

Cited by 89 publications

(58 citation statements)

References 24 publications

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“…Synergistic effects of IFN-␥ and TNF-␣ on FKN production have previously been described in human vascular smooth muscle cells and astrocytes (39,46,57). FKN production in other cell types, such as epithelial cells, endothelial cells, fibroblasts, and keratinocytes, can be induced by IFN-␥, TNF-␣, or IL-1␤ stimulation alone (7,9,21,25,26,34,41,43,54).…”

Section: Discussionmentioning

confidence: 85%

“…These include vascular endothelial cells (34), bronchial, intestinal, and renal tubular epithelial cells (7,25,43), vascular smooth muscle cells (8,9,39,46), dermal fibroblasts (21), astrocytes (57), and keratinocytes (54). A role for FKN-CX 3 CR1-mediated inflammation has been demonstrated in several inflammatory disorders such as rheumatoid arthritis (44,56), atherosclerosis (13,28), psoriasis (49), and various inflammatory conditions of the kidney, brain, and lung (12,25).…”

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confidence: 99%

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Fractalkine/CX₃CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

Sukkar

Issa

Xie

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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mokine synthesis by airway smooth muscle cells (ASMC) may be an important process underlying inflammatory cell recruitment in airway inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD). Fractalkine (FKN) is a recently described CX 3C chemokine that has dual functions, serving as both a cell adhesion molecule and a chemoattractant for monocytes and T cells, expressing its unique receptor, CX3CR1. We investigated FKN expression by human ASMC in response to the proinflammatory cytokines IL-1␤, TNF-␣, and IFN-␥, the T helper 2-type cytokines IL-4, IL-10, and IL-13, and the fibrogenic cytokine transforming growth factor (TGF)-␤. Neither of these cytokines alone had any significant effect on ASMC FKN production. Combined stimulation with IFN-␥ and TNF-␣ induced FKN mRNA and protein expression in a time-and concentration-dependent manner. TGF-␤ had a significant inhibitory effect on cytokine-induced FKN mRNA and protein expression. Dexamethasone (10 Ϫ8 -10 Ϫ6 M) significantly upregulated cytokineinduced FKN mRNA and protein expression. Finally, we used selective inhibitors of the mitogen-activated protein kinases c-Jun NH2-terminal kinase (JNK) (SP-610025), p38 (SB-203580), and extracellular signal-regulated kinase (PD-98095) to investigate their role in FKN production. SP-610025 (25 M) and SB-203580 (20 M), but not PD-98095, significantly attenuated cytokine-induced FKN protein synthesis. IFN-␥-and TNF-␣-induced JNK phosphorylation remained unaltered in the presence of TGF-␤ but was inhibited by dexamethasone, indicating that JNK is not involved in TGF-␤-or dexamethasone-mediated regulation of FKN production. In summary, FKN production by human ASMC in vitro is regulated by inflammatory and anti-inflammatory factors. chemokine; airway inflammation; asthma; chronic obstructive pulmonary disease THERE IS NOW SUBSTANTIAL EVIDENCE suggesting that airway smooth muscle cells (ASMC), by virtue of their immunomodulatory functions, may be involved in regulating airway inflammatory responses in diseases such as asthma and chronic obstructive pulmonary disease (COPD). ASMC express adhesion molecules and synthesize many cytokines and chemokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-8, eotaxin, and RANTES. These mediators are critically implicated in the recruitment, survival, and activation of key effector cells, such as eosinophils, neutrophils, and T lymphocytes, in asthma and COPD (10).Fractalkine (FKN), also known as CX 3 C ligand 1 (CX 3 CL1), is a novel chemokine belonging to the CX 3 C chemokine family. FKN is a multidomain molecule expressed on the cell surface and consists of a transmembrane region and a heavily glycosylated mucin-like stalk that extends from the cell surface, holding the chemokine domain at its tip (5). FKN also exists as a soluble glycoprotein that is generated by proteolytic cleavage of the full-length molecule at a membrane-proximal site (27,32,55). The physiological relevance of membrane and soluble FKN is not known; however, it is cu...

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Section: Discussionmentioning

confidence: 85%

mentioning

confidence: 99%

Fractalkine/CX₃CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

Sukkar

Issa

Xie

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…WY14643 and ciglitazone were from Calbiochem (San Diego, CA). Primer oligo(dT) [12][13][14][15][16][17][18] and MMulv reverse transcriptase were from Gibco-BRL (Gainthersburg, MD). RNeasy total RNA isolation kit and Taq DNA polymerase were purchased from Qiagen (Hilden, Germany).…”

Section: Reagentsmentioning

confidence: 99%

“…Single-strand cDNA for a PCR template was synthesized from 1 µ g of total RNA using a primer oligo(dT) [12][13][14][15][16][17][18] and M-Mulv reverse transcriptase under the conditions indicated by the manufacturer. Specific primers were designed from cDNA sequences for fractalkine, ICAM-1, VCAM-1, PPAR-α , PPAR-γ and glyceraldehyde-3-phosphate dehydrogenase (GAPDH).…”

Section: Rna Extraction Reverse Transcription-polymerase Chain Reactmentioning

confidence: 99%

“…14,15 Interferon-γ stimulates fractalkine expression in other types of cells such as bronchial epithelial cells 16 and brain astrocytes. 17 Fractalkine is incorporated into the cell surface membrane of activated endothelial cells and promotes strong adhesion of T lymphocytes and monocytes. 13 The soluble form of this chemokine is released from the membrane-bound molecules and serves as a chemoattractant for lymphocytes and monocytes.…”

Section: Introductionmentioning

confidence: 99%

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15‐Deoxy‐Δ^12,14‐prostaglandin J₂ inhibitsCX3CL1/fractalkine expression in human endothelial cells

Imaizumi¹,

Matsumiya

Tamo³

et al. 2002

Immunol Cell Biol

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Summary Peroxisome proliferator-activated receptor-γ (PPAR-γ ) is a member of nuclear hormone receptor superfamily, and is known to play a role in various biological processes including inflammatory responses and adipocyte differentiation. CX3CL1/fractalkine is a potent agonist for chemotaxis and adhesion of monocytes and lymphocytes. Endothelial cells produce fractalkine when stimulated with cytokines such as interleukin-1 (IL-1), tumour necrosis factor-α and interferon-γ (IFN-γ ). We herein report that 15-deoxy-᭝ 12,14 -prostaglandin J 2 (15d-PGJ 2 ), a PPAR-γ agonist, inhibits the expression of fractalkine induced by IFN-γ or IL-1 β in human endothelial cells. Agonist for PPAR-α (WY14643) or PPAR-γ (ciglitazone) did not inhibit the cytokine-induced fractalkine expression, and the effect of 15d-PGJ 2 may be independent of PPAR. 15-Deoxy-⌬ 12,14 prostaglandin J 2 also inhibited the adhesion of blood mononuclear cells to endothelial monolayers treated with IFN-γ or IL-1 β . The data suggest that 15d-PGJ 2 regulates inflammatory reactions, at least in part, through the inhibition of fractalkine expression and leucocyte traffic through the endothelium.

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Cytokine, chemokine and growth factor gene profiling of cultured human astrocytes after exposure to proinflammatory stimuli

Meeuwsen¹,

Persoon-Deen²,

Bsibsi³

et al. 2003

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166

131

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Astrocytes play key roles in CNS development, inflammation, and repair by producing a wide variety of cytokines, chemokines, and growth factors. Understanding the regulation of this network is important for a full understanding of astrocyte functioning. In this study, expression levels of 268 genes encoding cytokines, chemokines, growth factors, and their receptors were established in cultured human adult astrocytes using cDNA arrays. Also, changes in this gene profile were determined following stimulation with TNFalpha, IL-1beta, and IFNgamma. The data obtained reveal a highly reproducible pattern of gene expression not only between different astrocyte cultures from a single source, but also between astrocytes from different donors. They also identify several gene products not previously described for human astrocytes, including a.o. IL-17, CD70, CD147, and BIGH3. When stimulated with TNFalpha astrocytes respond with increased expression of several genes, notably including those encoding the chemokines CCL2 (MCP-1), CCL5 (RANTES), and CXCL8 (IL-8), growth factors including BMP-2A, BMP-3, neuromodulin (GAP43), BDNF, and G-CSF, and receptors such as the CRF receptor, the calcitonin receptor (CTR), and TKT. The response to IL-1beta involves largely the same range of genes, but responses were blunted in comparison to the TNFalpha response. Treatment with IFNgamma had no or only marginal effects on expression of any of the 268 genes analyzed. Astrocytes treated with a mixture of all three stimuli together displayed responses that are largely similar to those found in response to TNFalpha or IL-1beta alone, with only few additional synergistic effects.

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Synergistic stimulation, by tumor necrosis factor-α and interferon-γ, of fractalkine expression in human astrocytes

Cited by 89 publications

References 24 publications

Fractalkine/CX₃CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

Fractalkine/CX₃CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

15‐Deoxy‐Δ^12,14‐prostaglandin J₂ inhibitsCX3CL1/fractalkine expression in human endothelial cells

Cytokine, chemokine and growth factor gene profiling of cultured human astrocytes after exposure to proinflammatory stimuli

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Synergistic stimulation, by tumor necrosis factor-α and interferon-γ, of fractalkine expression in human astrocytes

Cited by 89 publications

References 24 publications

Fractalkine/CX3CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

Fractalkine/CX3CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

15‐Deoxy‐Δ12,14‐prostaglandin J2 inhibitsCX3CL1/fractalkine expression in human endothelial cells

Cytokine, chemokine and growth factor gene profiling of cultured human astrocytes after exposure to proinflammatory stimuli

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Fractalkine/CX₃CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

Fractalkine/CX₃CL1 production by human airway smooth muscle cells: induction by IFN-γ and TNF-α and regulation by TGF-β and corticosteroids

15‐Deoxy‐Δ^12,14‐prostaglandin J₂ inhibitsCX3CL1/fractalkine expression in human endothelial cells