Interleukin-1β and tumour necrosis factor-α promote the transformation of human immortalised mesothelial cells by erionite

Wang, Yaohe; Faux, Steven P.; Halldén, Gunnel; Kirn, David H.; Houghton, Cathy E.; Lemoine, Nicholas R.; Patrick, G.

doi:10.3892/ijo.25.1.173

Cited by 37 publications

(46 citation statements)

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“…(30) Activated macrophages secrete a panel of growth factors and cytokines to regulate cell proliferation, which can augment transformation of mesothelial cells. (28,30,32,33) Our observations that mesothelial cell proliferation is enhanced by conditioned macrophage culture media and by the supernatants of pleural cavity lavage are consistent with these results, although the factors that are involved need to be identified.…”

Section: Discussionsupporting

confidence: 83%

Multi‐walled carbon nanotubes translocate into the pleural cavity and induce visceral mesothelial proliferation in rats

et al. 2012

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Multi-walled carbon nanotubes have a fibrous structure similar to asbestos and induce mesothelioma when injected into the peritoneal cavity. In the present study, we investigated whether carbon nanotubes administered into the lung through the trachea induce mesothelial lesions. Male F344 rats were treated with 0.5 mL of 500 lg/mL suspensions of multi-walled carbon nanotubes or crocidolite five times over a 9-day period by intrapulmonary spraying. Pleural cavity lavage fluid, lung and chest wall were then collected. Multi-walled carbon nanotubes and crocidolite were found mainly in alveolar macrophages and mediastinal lymph nodes. Importantly, the fibers were also found in the cell pellets of the pleural cavity lavage, mostly in macrophages. Both multi-walled carbon nanotube and crocidolite treatment induced hyperplastic proliferative lesions of the visceral mesothelium, with their proliferating cell nuclear antigen indices approximately 10-fold that of the vehicle control. The hyperplastic lesions were associated with inflammatory cell infiltration and inflammationinduced fibrotic lesions of the pleural tissues. The fibers were not found in the mesothelial proliferative lesions themselves. In the pleural cavity, abundant inflammatory cell infiltration, mainly composed of macrophages, was observed. Conditioned cell culture media of macrophages treated with multi-walled carbon nanotubes and crocidolite and the supernatants of pleural cavity lavage fluid from the dosed rats increased mesothelial cell proliferation in vitro, suggesting that mesothelial proliferative lesions were induced by inflammatory events in the lung and pleural cavity and likely mediated by macrophages. In conclusion, intrapulmonary administration of multi-walled carbon nanotubes, like asbestos, induced mesothelial proliferation potentially associated with mesothelioma development. (Cancer Sci 2012; 103: 2045-2050 M ulti-walled carbon nanotubes (MWCNT) are structurally composed of cylinders rolled up from several layers of graphite sheets. They are several to tens of nanometers in diameter and several to tens of micrometers in length. This high length to diameter aspect ratio, a characteristic shared with asbestos fibers, has led to concern that exposure to MWCNT might cause asbestos-like lung diseases, such as lung fibrosis, lung cancer, pleural plaque and malignant mesothelioma.(1-6) Pleural plaque and malignant mesothelioma are characteristic lesions in asbestos-exposed humans. Although fiber dimensions, biopersistence, oxidative stress and inflammation have all been implicated, (7)(8)(9)(10)(11)(12) the exact mechanisms of pleural pathogenesis are unclear. According to a pathogenesis paradigm suggested by Donaldson et al.,asbestos fibers penetrate into the pleural cavity from the alveoli and deposit in the pleural tissue. Unlike spherical particles, fibrous materials such as asbestos are not cleared effectively from the pleural cavity, resulting in deposition of the fibers in the parietal pleura. This deposition, in turn, causes frustrated ...

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Section: Discussionsupporting

confidence: 83%

Multi‐walled carbon nanotubes translocate into the pleural cavity and induce visceral mesothelial proliferation in rats

et al. 2012

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“…TNF-a causes both apoptosis and compensatory proliferation in mesothelial cells (24). The fact that IL-1b and TNF-a contribute to mesothelial cell transformation (50) suggests that their importance in multiple stages of tumorigenesis may be due in part to activation of AP-1-or NF-kB-dependent gene expression. Moreover, it has recently been reported that NF-kB is a constitutive survival factor in human mesothelial cells exposed to asbestos and is up-regulated in MM cells (51).…”

Section: Asbestos Activates Nf-kb and The Tnf-a Receptormentioning

confidence: 99%

Asbestos, Lung Cancers, and Mesotheliomas

Heintz

Janssen–Heininger

Mossman

2010

Am J Respir Cell Mol Biol

160

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Fifteen years have passed since we published findings in the AJRCMB demonstrating that induction of early response fos/jun protooncogenes in rodent tracheal and mesothelial cells correlates with fibrous geometry and pathogenicity of asbestos. Our study was the first to suggest that the aberrant induction of signaling responses by crocidolite asbestos and erionite, a fibrous zeolite mineral associated with the development of malignant mesotheliomas (MMs) in areas of Turkey, led to altered gene expression. New data questioned the widely held belief at that time that the carcinogenic effects of asbestos in the development of lung cancer and MM were due to genotoxic or mutagenic effects. Later studies by our group revealed that proto-oncogene expression and several of the signaling pathways activated by asbestos were redox dependent, explaining why antioxidants and antioxidant enzymes were elevated in lung and pleura after exposure to asbestos and how they alleviated many of the phenotypic and functional effects of asbestos in vitro or after inhalation. Since these original studies, our efforts have expanded to understand the interface between asbestos-induced redox-dependent signal transduction cascades, the relationship between these pathways and cell fate, and the role of asbestos and cell interactions in development of asbestos-associated diseases. Of considerable significance is the fact that the signal transduction pathways activated by asbestos are also important in survival and chemoresistance of MMs and lung cancers. An understanding of the pathogenic features of asbestos fibers and dysregulation of signaling pathways allows strategies for the prevention and therapy of asbestos-related diseases.

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“…Among these cytokines, TNF-α has been identified as a critical mediator of the pathogenesis of asbestos-related disease. TNF-α has been linked to tumor promotion (10,11), fibrosis and asbestosis (10,12,13), asbestos carcinogenesis (14), and MM (10).…”

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confidence: 99%

Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation

Yang

Rivera

Jube

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

237

255

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Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic to human mesothelial cells (HM), which appears counterintuitive for a carcinogen. We show that asbestos-induced HM cell death is a regulated form of necrosis that links to carcinogenesis. Asbestos-exposed HM activate poly(ADP-ribose) polymerase, secrete H 2 O 2 , deplete ATP, and translocate high-mobility group box 1 protein (HMGB1) from the nucleus to the cytoplasm, and into the extracellular space. The release of HMGB1 induces macrophages to secrete TNF-α, which protects HM from asbestos-induced cell death and triggers a chronic inflammatory response; both favor HM transformation. In both mice and hamsters injected with asbestos, HMGB1 was specifically detected in the nuclei, cytoplasm, and extracellular space of mesothelial and inflammatory cells around asbestos deposits. TNF-α was coexpressed in the same areas. HMGB1 levels in asbestos-exposed individuals were significantly higher than in nonexposed controls (P < 0.0001). Our findings identify the release of HMGB1 as a critical initial step in the pathogenesis of asbestos-related disease, and provide mechanistic links between asbestos-induced cell death, chronic inflammation, and carcinogenesis. Chemopreventive approaches aimed at inhibiting the chronic inflammatory response, and especially blocking HMGB1, may decrease the risk of malignant mesothelioma among asbestos-exposed cohorts.mesothelioma | tumor necrosis factor-alpha | carcinogenesis | biomarker | chemoprevention

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Interleukin-1β and tumour necrosis factor-α promote the transformation of human immortalised mesothelial cells by erionite

Cited by 37 publications

References 0 publications

Multi‐walled carbon nanotubes translocate into the pleural cavity and induce visceral mesothelial proliferation in rats

Multi‐walled carbon nanotubes translocate into the pleural cavity and induce visceral mesothelial proliferation in rats

Asbestos, Lung Cancers, and Mesotheliomas

Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation

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