IL-17A stimulates granulocyte colony-stimulating factor production via ERK1/2 but not p38 or JNK in human renal proximal tubular epithelial cells

Hirai, Yuki; Iyoda, Masayuki; Shibata, Takanori; Kuno, Yoshinori; Kawaguchi, Mio; Hizawa, Nobuyuki; Matsumoto, Keīichi; Wada, Yukihiro; Kokubu, Fumio; Akizawa, Tadao

doi:10.1152/ajprenal.00113.2011

Cited by 21 publications

(17 citation statements)

References 35 publications

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“…The data are also consistent with our previous observations showing reductions in BAL G-CSF in O 3 -exposed adiponectin-deficient mice treated with anti-IL-17A [18]. The observed role of IL-17A in G-CSF expression is in agreement with previous reports indicating that IL-17A signaling increases the transcription and stability of the Gcsf mRNA [56], [57], via effects on ERK1/2 activation [58]. G-CSF causes neutrophil release from bone marrow and promotes neutrophil survival [59].…”

Section: Discussionsupporting

confidence: 93%

γδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFα

Mathews¹,

Williams²,

Brand³

et al. 2014

PLoS ONE

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Ozone is an air pollutant that causes pulmonary symptoms. In mice, ozone exposure causes pulmonary injury and increases bronchoalveolar lavage macrophages and neutrophils. We have shown that IL-17A is important in the recruitment of neutrophils after subacute ozone exposure (0.3 ppm for 24–72 h). We hypothesized that γδ T cells are the main producers of IL-17A after subacute ozone. To explore this hypothesis we exposed wildtype mice and mice deficient in γδ T cells (TCRδ−/−) to ozone or room air. Ozone-induced increases in BAL macrophages and neutrophils were attenuated in TCRδ−/− mice. Ozone increased the number of γδ T cells in the lungs and increased pulmonary Il17a mRNA expression and the number of IL-17A+ CD45+ cells in the lungs and these effects were abolished in TCRδ−/− mice. Ozone-induced increases in factors downstream of IL-17A signaling, including G-CSF, IL-6, IP-10 and KC were also decreased in TCRδ−/− versus wildtype mice. Neutralization of IL-17A during ozone exposure in wildtype mice mimicked the effects of γδ T cell deficiency. TNFR2 deficiency and etanercept, a TNFα antagonist, also reduced ozone-induced increases in Il17a mRNA, IL-17A+ CD45+ cells and BAL G-CSF as well as BAL neutrophils. TNFR2 deficient mice also had decreased ozone-induced increases in Ccl20, a chemoattractant for IL-17A+ γδ T cells. Il17a mRNA and IL-17A+ γδ T cells were also lower in obese Cpefat versus lean WT mice exposed to subacute ozone, consistent with the reduced neutrophil recruitment observed in the obese mice. Taken together, our data indicate that pulmonary inflammation induced by subacute ozone requires γδ T cells and TNFα-dependent recruitment of IL-17A+ γδ T cells to the lung.

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Section: Discussionsupporting

confidence: 93%

γδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFα

Mathews¹,

Williams²,

Brand³

et al. 2014

PLoS ONE

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“…Cells were grown in DMEM containing 10% fetal bovine serum (FBS), a 1% streptomycin-penicillin mixture, 44 mM NaHCO3, and 14 mM HEPES in an atmosphere of 5% CO2 and 95% air at 37°C in a humidified incubator. Experiments were performed with cells up to the fifth passage, as it has been shown that there are no phenotypic changes up to this passage number [21].…”

Section: Methodsmentioning

confidence: 99%

Epidermal Growth Factor Receptor Inhibition with Erlotinib Partially Prevents Cisplatin-Induced Nephrotoxicity in Rats

et al. 2014

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The effects of blocking the epidermal growth factor receptor (EGFR) in acute kidney injury (AKI) are controversial. Here we investigated the renoprotective effect of erlotinib, a selective tyrosine kinase inhibitor that can block EGFR activity, on cisplatin (CP)-induced AKI. Groups of animals were given either erlotinib or vehicle from one day before up to Day 3 following induction of CP- nephrotoxicity (CP-N). In addition, we analyzed the effects of erlotinib on signaling pathways involved in CP-N by using human renal proximal tubular cells (HK-2). Compared to controls, rats treated with erlotinib exhibited significant improvement of renal function and attenuation of tubulointerstitial injury, and reduced the number of apoptotic and proliferating cells. Erlotinib-treated rats had a significant reduction of renal cortical mRNA for profibrogenic genes. The Bax/Bcl-2 mRNA and protein ratios were significantly reduced by erlotinib treatment. In vitro, we observed that erlotinib significantly reduced the phosphorylation of MEK1 and Akt, processes that were induced by CP in HK-2. Taken together, these data indicate that erlotinib has renoprotective properties that are likely mediated through decreases in the apoptosis and proliferation of tubular cells, effects that reflect inhibition of downstream signaling pathways of EGFR. These results suggest that erlotinib may be useful for preventing AKI in patients receiving CP chemotherapy.

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“…Studies in human renal proximal tubule epithelial cells and models of renal inflammation show that IL‐17 stimulates production of chemokines, cytokines, angiogenic factors and granulopoietic growth factors through upregulation of numerous proinflammatory and profibrotic genes and alteration of genes associated with extracellular matrix remodelling and cell‐cell interactions . In Th17‐mediated kidney injury, infiltrating Th17 cells secrete IL‐17, which stimulates resident renal proximal tubular epithelial cells to produce IL‐6, C‐X‐C motif ligand (CXCL) 8, C‐C motif ligand (CCL) 2 and other chemokines and inflammatory mediators.…”

Section: Cellular Effects Of Il‐17mentioning

confidence: 99%

Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities

Krueger

Brunner

2017

Experimental Dermatology

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Psoriasis is a chronic, immune-mediated, systemic inflammatory disease that is defined by a characteristic skin reaction produced when elevated levels of inflammatory cytokines such as interleukin (IL)-17 alter the growth and differentiation of skin cells.The pathogenesis of comorbid conditions associated with psoriasis, including psoriatic arthritis, cardiovascular disease, obesity, metabolic syndrome, liver disorders, renal disease and depression, is also largely affected by inflammation. In this review, we examine the effect of IL-17 on the inflammatory pathways in a variety of different cell types, including keratinocytes, as well as epithelial cells of the colon, kidney, gut and liver. Additionally, we investigate the role of IL-17 in mediating the psoriasis-associated comorbidities detailed above. K E Y W O R D Scardiovascular disease, keratinocyte, metabolic syndrome, obesity, review

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IL-17A stimulates granulocyte colony-stimulating factor production via ERK1/2 but not p38 or JNK in human renal proximal tubular epithelial cells

Abstract: Akizawa T. IL-17A stimulates granulocyte colony-stimulating factor production via ERK1/2 but not p38 or JNK in human renal proximal tubular epithelial cells.

Cited by 21 publications

References 35 publications

γδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFα

γδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFα

Epidermal Growth Factor Receptor Inhibition with Erlotinib Partially Prevents Cisplatin-Induced Nephrotoxicity in Rats

Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities

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