Environmental risk factors of systemic sclerosis

Marie, I.; Gehanno, Jean-François

doi:10.1007/s00281-015-0507-3

Cited by 51 publications

(38 citation statements)

References 112 publications

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“…Scleroderma onset is linked to occupational exposure including exposure to organic solvents such as trichloroethylene, working with polyvinyl chloride, and silica dust exposure (Stephens et al, 1994, Englert et al, 2005, Marie and Gehanno, 2015. Furthermore certain geographical clusters have been described in keeping with an environmental initiating factor.…”

Section: Initiation Of Tissue Injury In Sclerodermamentioning

confidence: 99%

Chemokines in systemic sclerosis

2018

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Section: Initiation Of Tissue Injury In Sclerodermamentioning

confidence: 99%

Chemokines in systemic sclerosis

2018

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“…The pathogenic mechanisms of crystalline silica in the development of SSc remain unclear [27]. Silica is known to be a T cell adjuvant.…”

Section: State Of Knowledge -Silicamentioning

confidence: 99%

Potential occupational and environmental factors in SSc onset

Walecka¹,

Roszkiewicz²,

Malewska³

2018

Ann Agric Environ Med.

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Introduction and objective. Systemic sclerosis [SSc; scleroderma] is a rare, connective tissue disorder affecting all organs and systems. The primary feature of this disease is a chronic, progressive fibrosis due to excessive production of collagen and other components. There are two subsets of systemic sclerosis: 1) diffused SSc (dSSc), 2) limited SSc (lSSc) and 3) scleroderma without sclerosis (SSSC). The presented review is an attempt to summarize recent data regarding environmental and occupational factors in SSc onset. State of knowledge. There are many factors to be taken under consideration with SSc onset, although a strong correlation has been established for only a few. The most distinct factors are: crystalline silica and organic solvents (such as white spirit, aromatic, aliphatic-chain, chlorinated solvents, ketones, welding fumes). For other factors, which include abstestos, air pollution, other chemicals, silicone breast implants, tobacco smoking, drug reactions, diet influence and exposure to heavy metals, the jury is still out, and their position in SSc onset needs further studies. Conclusions. Although the pathogenesis of scleroderma remains unclear, there is a marked correlation between the onset of SSc and certain environmental or occupational factors.

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“…In addition to genetic factors, environmental factors are also thought to be important for triggering the disease progression of CTDs [3,4]. For example, occupational exposure to silica, asbestos, organic solvents such as trichloroethylene, and aromatic solvents are risk factors for systemic sclerosis, a prototype CTD with systemic fibrosis, including ILD [5,6]. Further, cigarette smoking is strongly associated with the disease progression of rheumatoid arthritis with ILD [7].…”

Section: Introductionmentioning

confidence: 99%

Aryl hydrocarbon receptor signals attenuate lung fibrosis in the bleomycin-induced mouse model for pulmonary fibrosis through increase of regulatory T cells

et al. 2020

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Background: Interstitial lung disease (ILD) is a serious complication of connective tissue diseases (CTDs). Although immune dysregulation triggered by genetic and environmental factors is thought to provoke inflammation and subsequent fibrosis, precise mechanisms of these processes remain unclear. Recent reports suggest that activation of aryl hydrocarbon receptor (AhR) signals by various ligands such as tryptophan derivatives can induce hyperimmune responses and are involved in autoimmunity. We investigated the effects of AhR signals on the process of lung fibrosis and changes in immunological features using a bleomycin (BLM)-induced lung fibrosis mouse model. Methods: BLM was administered intratracheally to C57BL/6JJcl mice and either 5,11-dihydroindolo[3,2-b]carbazole-6-carboxaldehyde (FICZ), a natural AhR ligand, or vehicle was subsequently injected intraperitoneally on day 0, 1, and 2 from BLM administration. Mice were sacrificed at week 3, and lung fibrosis was quantified by the histological changes using the Ashcroft score and deposition of soluble collagen levels in the lung using Sircol assay. The population of immune cells infiltrated into the lungs was analyzed using flow cytometry.Results: Both the Ashcroft score and soluble collagen level in FICZ-treated mice were significantly lower than those in the vehicle group. Moreover, the survival rate of FICZ-treated mice was significantly higher than that of control mice during the 3 weeks after treatment. Interestingly, flow cytometric analysis revealed that the number of CD4 + Foxp3 + regulatory T cells (Tregs) was significantly increased and CD4 + IFNγ + and γδ + IL-17A + T cells were decreased in the lungs of FICZ-treated mice, while the total number of T, B, and NK cells were unaffected by FICZ treatment.Conclusions: Our findings suggest that stimulation of AhR signals attenuated lung fibrosis by increasing Tregs and suppressing inflammatory T cell subsets in a BLM-induced fibrosis model. AhR signaling pathways may therefore be useful therapeutic targets for connective tissue disease-associated ILD.

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Environmental risk factors of systemic sclerosis

Cited by 51 publications

References 112 publications

Chemokines in systemic sclerosis

Chemokines in systemic sclerosis

Potential occupational and environmental factors in SSc onset

Aryl hydrocarbon receptor signals attenuate lung fibrosis in the bleomycin-induced mouse model for pulmonary fibrosis through increase of regulatory T cells

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