Pulmonary overexpression of IL-10 augments lung fibrosis and Th2 responses induced by silica particles

Barbarin, Virginie; Xing, Zhou; Delos, Monique; Lison, Dominique; Huaux, François

doi:10.1152/ajplung.00329.2004

Cited by 106 publications

(82 citation statements)

References 64 publications

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“…Thus, it remains to be explained why chronic lung inflammation induced by silica is not directed by IL-17-producing T cells as it is during the earlier response. We demonstrated previously that long-term responses to silica in mice are strongly associated with the upregulation of suppressive cytokines, such as IL-10, which control, at least in part, the establishment of chronic inflammation (24,57). Thus, we can speculate that this anti-inflammatory response can control the proinflammatory activities of IL-17A, as demonstrated in several recent reports (13,(58)(59)(60).…”

Section: Discussionsupporting

confidence: 59%

IL-17A–Producing γδ T and Th17 Lymphocytes Mediate Lung Inflammation but Not Fibrosis in Experimental Silicosis

Re¹,

Dumoutier

Couillin

et al. 2010

The Journal of Immunology

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130

107

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IL-17–producing T lymphocytes play a crucial role in inflammation, but their possible implication in fibrosis remains to be explored. In this study, we examined the involvement of these cells in a mouse model of lung inflammation and fibrosis induced by silica particles. Upregulation of IL-17A was associated with the development of experimental silicosis, but this response was markedly reduced in athymic, γδ T cell-deficient or CD4+ T cell-depleted mice. In addition, γδ T lymphocytes and CD4+ T cells, but not macrophages, neutrophils, NK cells or CD8 T cells, purified from the lungs of silicotic mice markedly expressed IL-17A. Depletion of alveolar macrophages or neutralization of IL-23 reduced upregulation of IL-17A in the lung of silicotic mice. IL-17R–deficient animals (IL-17R−/−) or IL-17A Ab neutralization, but not IL-22−/− mice, developed reduced neutrophil influx and injury during the early lung response to silica. However, chronic inflammation, fibrosis, and TGF-β expression induced by silica were not attenuated in the absence of IL-17R or -22 or after IL-17A Ab blockade. In conclusion, a rapid lung recruitment of IL-17A–producing T cells, mediated by macrophage-derived IL-23, is associated with experimental silicosis in mice. Although the acute alveolitis induced by silica is IL-17A dependent, this cytokine appears dispensable for the development of the late inflammatory and fibrotic lung responses to silica.

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Section: Discussionsupporting

confidence: 59%

IL-17A–Producing γδ T and Th17 Lymphocytes Mediate Lung Inflammation but Not Fibrosis in Experimental Silicosis

Re¹,

Dumoutier

Couillin

et al. 2010

The Journal of Immunology

Self Cite

130

107

View full text Add to dashboard Cite

show abstract

“…The results from the study evidenced acute pulmonary inflammation and neutrophil infiltration to the lung tissues in a dose-dependent manner [193]. Similar studies using silica nanoparticles reported induction of anti-inflammatory mediators and reversibility of fibrotic changes [194,195]. A few studies in lung tissues suspected translocation and diffusion of silica nanoparticles away from the lung tissue through systematic circulation and deposition in extra pulmonary organs [196][197][198].…”

Section: Effects On Organ Systemsmentioning

confidence: 55%

“…The toxicity of the titanium oxide nanoparticle was observed when keratinocyte cell line (HaCaT), human dermal fibroblasts and human immortalized sebaceous gland cell lines (SZ95) were used. The cytotoxicity affected cellular functions including differentiation, cell proliferation and mobility which resulted in apoptosis [220].Upregulation of fibrogenic mediators including IL-4, IL-10 and IL-13 was also observed contributing to fibrotic changes [195].…”

Section: Mechanistic Studiesmentioning

confidence: 99%

In vitro and in vivo toxicity assessment of nanoparticles

2017

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Nanotechnology has revolutionized gene therapy, diagnostics and environmental remediation. Their bulk production, uses and disposal have posed threat to the environment. With the appearance of these nanoparticles in the environment, their toxicity assessment is an immediate concern. This review is an attempt to summarize the major techniques used in cytotoxity determination. The review also presents a detailed and elaborative discussion on the toxicity imposed by different types of nanoparticles including carbon nanotubes, gold nanoparticles, silver nanoparticles, quantum dots, fullerenes, aluminium nanoparticles, zinc nanoparticles, iron nanoparticles, titanium nanoparticles and silica nanoparticles. It discusses the in vitro and in vivo toxological effects of nanoparticles on bacteria, microalgae, zebrafish, crustacean, fish, rat, mouse, pig, guinea pig, human cell lines and human. It also discusses toxological effects on organs such as liver, kidney, spleen, sperm, neural tissues, liver lysosomes, spleen macrophages, glioblastoma cells, hematoma cells and various mammalian cell lines. It provides information about the effects of nanoparticles on the gene-expression, growth and reproduction of the organisms.

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“…Although delivery of IL-10 plasmid inhibits bleomycininduced pulmonary fibrosis [27], transgenic mice over expressing IL-10 develop pulmonary inflammation and subepithelial fibrosis with an accumulation of TGF-b1 [28]. In accordance, IL-10 augments the fibrotic responses to inhaled silica particles as seen in IL-10 deficient mice [29] and over expression of IL-10 by adenoviral gene transfer [30]. In vitro, IL-10 also induces TGF-b1 expression in alveolar macrophages [29].…”

Section: Discussionmentioning

confidence: 94%

Suberoylanilide hydroxamic acid: a potential epigenetic therapeutic agent for lung fibrosis?

Wang¹,

C²,

Finger³

et al. 2009

European Respiratory Journal

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Pulmonary fibrosis represents a fatal stage of interstitial lung diseases of known and idiopathic aetiology. No effective therapy is currently available. Based on an indication-discovery approach we present novel in vitro evidence that the histone deacetylases inhibitor suberoylanilide hydroxamic acid (SAHA), an FDA approved anti-cancer drug, has antifibrotic and anti-inflammatory potential.Human lung fibroblasts (fetal, adult and idiopathic adult pulmonary fibrosis) were treated with transforming growth factor (TGF)-b1 with or without SAHA. Collagen deposition, a-smooth muscle actin (a-SMA) expression, matrix metalloproteinase (MMP)1 activity, tissue inhibitor of MMP (TIMP)1 production, apoptosis and cell proliferation were assessed. Pro-inflammatory cytokines relevant to pulmonary fibrosis were assayed in SAHA-treated human peripheral blood mononuclear cells (PBMC) and its subpopulations.SAHA abrogated TGF-b1 effects on all the fibroblast lines by preventing their transdifferentiation into a-SMA positive myofibroblasts and increased collagen deposition without inducing apoptosis. However, MMP1 activity and TIMP1 production was modulated without a clear fibrolytic effect. SAHA also inhibited serum-induced proliferation of the fibroblast lines and caused hyperacetylation of a-tubulin and histone. Cytokine secretion was inhibited from PBMC and lymphocytes at nonapoptotic concentrations.Taken together, these data demonstrate combined antifibrotic and anti-inflammatory properties of SAHA, suggesting its therapeutic potential for pulmonary fibrosis.

show abstract

Pulmonary overexpression of IL-10 augments lung fibrosis and Th2 responses induced by silica particles

Abstract: Barbarin, Virginie, Zhou Xing, Monique Delos, Dominique Lison, and Francois Huaux. Pulmonary overexpression of IL-10 augments lung fibrosis and Th2 responses induced by silica particles.

Cited by 106 publications

References 64 publications

IL-17A–Producing γδ T and Th17 Lymphocytes Mediate Lung Inflammation but Not Fibrosis in Experimental Silicosis

IL-17A–Producing γδ T and Th17 Lymphocytes Mediate Lung Inflammation but Not Fibrosis in Experimental Silicosis

In vitro and in vivo toxicity assessment of nanoparticles

Suberoylanilide hydroxamic acid: a potential epigenetic therapeutic agent for lung fibrosis?

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