Thalidomide reduces IL-18, IL-8 and TNF-α release from alveolar macrophages in interstitial lung disease

Ye, Q; Chen, B; Tong, Zhaohui; Nakamura, Shinobu; Sarrı́a, R.; Costabel, Ulrich; Guzman, Josune

doi:10.1183/09031936.06.00131505

Cited by 68 publications

(43 citation statements)

References 36 publications

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“…Because TGF-␤ 1 does not stimulate the proliferation of ␣-SMA-positive myofibroblasts, we propose a dual inhibitory effect of Thal on IL-6-dependent proliferation and TGF-␤ 1 -dependent transdifferentiation of fibroblasts to myofibroblast, which may be the mechanism underlying the preventive and therapeutic effect of Thal on pulmonary fibrosis. Recently it has been reported that Thal reduced the production of TNF-␣, IL-8, and IL-18 from alveolar macrophages in pulmonary fibrosis (48). Especially as to TNF-␣, Thal has been reported to reduce its production in damaged lung (49,50).…”

Section: Discussionmentioning

confidence: 99%

Thalidomide Prevents Bleomycin-Induced Pulmonary Fibrosis in Mice

Tabata

Kadokawa

et al. 2007

The Journal of Immunology

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Pulmonary fibrosis in humans can occur as a result of a large number of conditions. In idiopathic pulmonary fibrosis (IPF), pulmonary function becomes progressively compromised resulting in a high mortality rate. Currently there are no proven effective treatments for IPF. We have recently reported that IL-6 and TGF-β1 plays an important role in proliferation and differentiation of lung fibroblasts, and all-trans-retinoic acid (ATRA) prevented bleomycin-induced lung fibrosis through the inhibition of these cytokines. Thalidomide (Thal) has been used in the treatment of multiple myeloma through the inhibitory effect on IL-6-dependent cell growth and angiogenesis. In this study, we examined the preventive effect of Thal on bleomycin-induced pulmonary fibrosis in mice. We performed histological examinations and quantitative measurements of IL-6, TGF-β1, collagen type Iα1 (COL1A1), vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) in bleomycin-treated mouse lung tissues with or without the administration of Thal. Thal histologically ameliorated bleomycin-induced fibrosis in mouse lung tissues. Thal decreased the expressions of IL-6, TGF-β1, VEGF, Ang-1 Ang-2, and COL1A1 mRNA in mouse lung tissues. In addition, Thal inhibited angiogenesis in the lung. In vitro studies disclosed that Thal reduced 1) production of IL-6, TGF-β1, VEGF, Ang-1, and collagen synthesis from human lung fibroblasts, and 2) both IL-6-dependent proliferation and TGF-β1-dependent transdifferentiation of the cells, which could be the mechanism underlying the preventive effect of Thal on pulmonary fibrosis. These data may provide a rationale to explore clinical use of Thal for the prevention of pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%

Thalidomide Prevents Bleomycin-Induced Pulmonary Fibrosis in Mice

Tabata

Kadokawa

et al. 2007

The Journal of Immunology

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“…However, while one report has described that thalidomide inhibits IL-6, 12 another has described that thalidomide does not affect IL-6. 13 Since we did not measure IL-6 in this case, we were not able to draw any conclusions on this issue. Therefore, further analysis is required in the future.…”

Section: Discussionmentioning

confidence: 90%

A Case of Extramedullary Plasmablastic Plasmacytoma Successfully Treated Using a Combination of Thalidomide and Dexamethasone and a Review of the Medical Literature

Sekiguchi

Asahina

Shimada³

et al. 2013

J Clin Exp Hematopathol

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A 56-year-old man developed epistaxis, hoarseness, and swelling of a finger in March 2010. On the basis of biopsies of the masses in the pharynx and finger, he was diagnosed with extramedullary plasmablastic plasmacytoma, with somewhat immature CD45 + , MPC-1 − , and CD49e −. CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisolone) and VCAP (vincristine, cyclophosphamide, doxorubicin, and prednisolone) therapy was ineffective, but combination therapy with thalidomide and dexamethasone was highly effective. Thalidomide monotherapy successfully maintained partial remission for approximately 7 months. A mass appeared in the right neck in February 2011, and a biopsy confirmed recurrence. Changes to CD45 negativity and MPC-1 partial positivity were seen, while CD49e negativity persisted, suggesting that the plasmablastic plasmacytoma had reverted to a more immature state. Bortezomib therapy was started in March 2011 and was effective. However, during the second round of treatment, the patient developed acute lung injury, which was improved by steroid pulse therapy. After the discontinuation of bortezomib, the extramedullary mass increased rapidly, and the patient died of multiple organ failure. An autopsy showed that plasmablastic plasmacytomas had infiltrated into multiple organs. Extramedullary plasmacytomas and those that revert to an immature state are associated with a poor prognosis, so further treatment improvements are needed in the future. 〔J Clin Exp Hematop 53(1): 21-28, 2013〕

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“…Macrophages are key inflammatory cells that have been documented to play a critical role in various airway disorders [13] . Upon stimulation with molecules such as LPS, these cells secrete an array of pro-inflammatory cytokines and oxidants, including TNF-α, IL-1β, and macrophage inflammatory protein-2 [14] . These proinflammatory cytokines genes are regulated by various transcription factors, including Egr-1 and NF-κB [15][16][17] .…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of 1,8-cineol (eucalyptol) on Egr-1 expression in lipopolysaccharide-stimulated THP-1 cells

Zhou

Wang

Tang

et al. 2007

Acta Pharmacologica Sinica

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Aim: To study the effects of 1,8‐cineol (eucalyptol) on the expression of early growth response factor‐1 (Egr‐1) and NF‐κB in the human monocyte THP‐1 cell line stimulated by lipopolysaccharide (LPS). Methods: The THP‐1 cells were incubated with serial doses of 1,8‐cineol (1, 10, and 100 mg/L, 30 min) before being stimulated with LPS (1 mg/L, 30 min). The localization of Egr‐1 in the THP‐1 cells was detected by immunofluorescence and a laser scanning confocal microscope. The expression of Egr‐1 in the nuclei and whole cell, and NF‐κB in the nuclei, were measured by Western blot analysis. Results: When stimulated by LPS, the FITC‐labeled Egr‐1 was detected mainly in the nuclei. Moreover, the expression of Egr‐1 in the whole cell increased markedly compared with the control cells. 1,8‐Cineol pretreatment decreased the expression of Egr‐1 in both the nuclei and whole cell of the LPS‐stimulated THP‐1 cells, and this effect was concentration‐dependent, but there was no reaction on the expression of NF‐κB in the nuclei protein in the LPS‐stimulated THP‐1 cells. Conclusion: In a concentration‐dependent manner, 1,8‐Cineol reduces LPS‐induced Egr‐1 expression in nuclei and in whole cell of THP‐1 cells, but shows no effect on NF‐κB expression.

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Thalidomide reduces IL-18, IL-8 and TNF-α release from alveolar macrophages in interstitial lung disease

Cited by 68 publications

References 36 publications

Thalidomide Prevents Bleomycin-Induced Pulmonary Fibrosis in Mice

Thalidomide Prevents Bleomycin-Induced Pulmonary Fibrosis in Mice

A Case of Extramedullary Plasmablastic Plasmacytoma Successfully Treated Using a Combination of Thalidomide and Dexamethasone and a Review of the Medical Literature

Inhibitory effect of 1,8-cineol (eucalyptol) on Egr-1 expression in lipopolysaccharide-stimulated THP-1 cells

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