TWEAK/Fn14 interaction stimulates human bronchial epithelial cells to produce IL-8 and GM-CSF

Xu, Hong-Ri; Okamoto, Atsushi; Ichikawa, Junichiro; Ando, Takashi; Tasaka, Kachio; Masuyama, Keisuke; Ogawa, Hideoki; Yagita, Hideo; Okumura, Ko; Nakao, Akihiro

doi:10.1016/j.bbrc.2004.04.036

Cited by 66 publications

(59 citation statements)

References 17 publications

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“…8A). The relatively delayed kinetics of TWEAK-induced I B-␣ phosphorylation in mesangial cells, as compared with that induced by TNF-␣, has been reported also in bronchial epithelial cells (14).…”

Section: Tweak Treatment Of Mesangial Cells Induces Phosphorylation Omentioning

confidence: 68%

“…In synoviocytes and fibroblasts, PGE 2 , MMP-1, IL-8, CCL5/RANTES, and CXCL10/IP-10 induction were seen (13). TWEAK treatment stimulates the secretion of IL-8 and GM-CSF from bronchial epithelial cells (14), and of CCL5/RANTES (but not CCL2/MCP-1 or IL-8) from keratinocytes (4). Finally, proinflammatory effects induced by TWEAK were also reported in astrocytes (42) and macrophages (15).…”

Section: Discussionmentioning

confidence: 99%

“…To investigate whether TWEAK-induced chemokine secretion seen in mesangial cells is mediated by NF-B activation or whether there is a major contribution of other signaling pathways (7), we treated mesangial cells with BAY11-7082 (E-3-(4-methylphenylsulfonyl)-2-propenenitrile; Calbiochem), an I B-␣ phosphorylation inhibitor (25), at 5 M for 30 min before TWEAK stimulation (14). Treatment of mesangial cells with BAY11-7082 significantly reduces chemokine production in response to TWEAK (Fig.…”

Section: Tweak Treatment Of Mesangial Cells Induces Phosphorylation Omentioning

confidence: 99%

“…In HUVECs, TWEAK (alone or in combination with other growth factors) enhances cell proliferation, migration, and resistance to apoptosis, and induces ICAM-1, Eselectin, CCL2/MCP-1, and IL-8 expression (9 -12). Proinflammatory cytokine secretion has also been recently described following TWEAK stimulation of synoviocytes, fibroblasts (13), bronchial epithelial cells (14), and macrophages (15).…”

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confidence: 93%

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Proinflammatory Effects of Tweak/Fn14 Interactions in Glomerular Mesangial Cells

Campbell

Burkly

Gao

et al. 2006

The Journal of Immunology

152

187

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TNF-like weak inducer of apoptosis, or TWEAK, is a relatively new member of the TNF-ligand superfamily. Ligation of the TWEAK receptor Fn14 by TWEAK has proinflammatory effects on fibroblasts, synoviocytes, and endothelial cells. Several of the TWEAK-inducible cytokines are important in the pathogenesis of kidney diseases; however, whether TWEAK can induce a proinflammatory effect on kidney cells is not known. We found that murine mesangial cells express cell surface TWEAK receptor. TWEAK stimulation of mesangial cells led to a dose-dependent increase in CCL2/MCP-1, CCL5/RANTES, CXCL10/IFN-γ-induced protein 10 kDa, and CXCL1/KC. The induced levels of chemokines were comparable to those found following mesangial cell exposure to potent proinflammatory stimuli such as TNF-α + IL-1β. CXCL11/interferon-inducible T cell α chemoattractant, CXCR5, mucosal addressin cell adhesion molecule-1, and VCAM-1 were up-regulated by TWEAK as well. TWEAK stimulation of mesangial cells resulted in an increase in phosphorylated Iκ-B, while pretreatment with an Iκ-B phosphorylation inhibitor significantly blocked chemokine induction, implicating activation of the NF-κB signaling pathway in TWEAK-induced chemokine secretion. Importantly, the Fn14-mediated proinflammatory effects of TWEAK on kidney cells were confirmed using mesangial cells derived from Fn14-deficient mice and by injection in vivo of TWEAK into wild-type vs Fn14-deficient mice. Finally, TWEAK-induced chemokine secretion was prevented by treatment with novel murine anti-TWEAK Abs. We conclude that TWEAK induces mesangial cells to secrete proinflammatory chemokines, suggesting a prominent role for TWEAK in the pathogenesis of renal injury. Our results support Ab inhibition of TWEAK as a potential new approach for the treatment of chemokine-dependent inflammatory kidney diseases.

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Section: Tweak Treatment Of Mesangial Cells Induces Phosphorylation Omentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Tweak Treatment Of Mesangial Cells Induces Phosphorylation Omentioning

confidence: 99%

mentioning

confidence: 93%

See 2 more Smart Citations

Proinflammatory Effects of Tweak/Fn14 Interactions in Glomerular Mesangial Cells

Campbell

Burkly

Gao

et al. 2006

The Journal of Immunology

152

187

View full text Add to dashboard Cite

show abstract

“…For example, TWEAK has been reported to stimulate cell proliferation (9 -12), migration (10,11,13), and differentiation (14). Also, TWEAK treatment of several different cell types induces the expression of proinflammatory molecules (5,10,(15)(16)(17)(18). TWEAK activity is mediated via binding to Fn14 (19), a member of the tumor necrosis factor receptor superfamily (6,7).…”

Section: Introductionmentioning

confidence: 99%

Soluble Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Overexpression in HEK293 Cells Promotes Tumor Growth and Angiogenesis in Athymic Nude Mice

Vu²,

Brown³

et al. 2004

Cancer Research

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Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the tumor necrosis factor superfamily of structurally related cytokines. TWEAK acts on responsive cells via binding to a cell surface receptor named Fn14. Recent studies have demonstrated that TWEAK can stimulate numerous cellular responses including cell proliferation, migration, and proinflammatory molecule production. It has also been reported that TWEAK can stimulate blood vessel formation in the rat cornea angiogenesis assay, but it is presently unknown whether this cytokine could play a role in the pathological angiogenesis associated with human diseases such as cancer, rheumatoid arthritis, and diabetic retinopathy. In the present study we investigated whether TWEAK was expressed in human tumors and whether it could promote tumor growth and angiogenesis in vivo. TWEAK mRNA expression was detected in many tumor types by cDNA array hybridization analysis, and TWEAK protein expression was confirmed in human colon cancer tissue by immunohistochemistry. As an initial approach to address whether TWEAK might act as a tumor angiogenesis factor, we established several human embryonic kidney cell lines that constitutively secrete a soluble TWEAK protein and examined their growth properties in vitro and in vivo. We found that although TWEAK-overexpressing cells do not have a growth advantage in vitro, they form larger and more highly vascularized tumors in athymic mice when compared with control, vector-transfected cells. This result suggests that the TWEAK-Fn14 signaling system may be a potential regulator of human tumorigenesis.

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Soluble TWEAK is markedly elevated in hemophagocytic lymphohistiocytosis

et al. 2007

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Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a newly identified monocyte derived cytokine, which has weak apoptosis inducing function against sensitive tumor cell lines in vitro. Also, TWEAK has been reported to have proangiogenic and proinflammatory activities in vivo. However, its functions in pathological situation remain to be elucidated. Here, we analyzed soluble TWEAK in serum of 24 patients with hemophagocytic lymphohistiocytosis (HLH) in combination with interferon-c (IFN-c) and killer-specific secretory protein of 37 kDa (Ksp37). Soluble TWEAK was not detected in serum of healthy individuals. Soluble TWEAK was markedly elevated in all six primary HLH patients and 12 of 18 secondary HLH patients. Serum IFN-c, which is an only known mediator to stimulate TWEAK production in monocyte in vitro, was not elevated despite elevated serum TWEAK in three of six primary HLH patients, although IFN-c was markedly elevated in other cases. Ksp37 was only slightly increased in HLH patients. These results indicate that TWEAK may be involved in pathogenesis of HLH and is useful as a clinical marker. Am. J. Hematol. 83:222-225, 2008. V

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TWEAK/Fn14 interaction stimulates human bronchial epithelial cells to produce IL-8 and GM-CSF

Cited by 66 publications

References 17 publications

Proinflammatory Effects of Tweak/Fn14 Interactions in Glomerular Mesangial Cells

Proinflammatory Effects of Tweak/Fn14 Interactions in Glomerular Mesangial Cells

Soluble Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Overexpression in HEK293 Cells Promotes Tumor Growth and Angiogenesis in Athymic Nude Mice

Soluble TWEAK is markedly elevated in hemophagocytic lymphohistiocytosis

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