Silica‐related diseases in the modern world: A role for self‐DNA sensing in lung inflammatory diseases

Togbé, Dieudonnée; Benmerzoug, Sulayman; Jacobs, Muazzam; Ryffel, Bernhard; Quesniaux, Valérie

doi:10.1111/all.14463

Cited by 4 publications

(3 citation statements)

References 6 publications

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“…Occupational exposure to crystalline silica dust has been identified as a major cause of chronic inflammation, fibrosis, cancer and autoimmune diseases (Hoy and Chambers 2020;Togbe et al, 2020). Compared with crystalline, amorphous silica has been generally considered safe.…”

Section: The "Previous" Model Elucidating the Proinflammatory Activit...mentioning

confidence: 99%

Think Beyond Particle Cytotoxicity: When Self-Cellular Components Released After Immunogenic Cell Death Explain Chronic Disease Development

Leinardi

Sanchez-Calero²,

Huaux³

2022

Front. Toxicol.

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The prolonged perturbation of the immune system following the release of a plethora of self-molecules (known as damage-associated molecular patterns, DAMPs) by stressed or dying cells triggers acute and chronic pathological responses. DAMPs are commonly released after plasma membrane damage or complete rupture due to immunogenic cell death (ICD), upon numerous stressors including infectious and toxic agents. The set of DAMPs released after ICD include mature proinflammatory cytokines and alarmins, but also polymeric macromolecules. These self-intracellular components are recognized by injured and healthy surrounding cells via innate receptors, and induce upregulation of stress-response mechanisms, including inflammation. In this review, by overstepping the simple toxicological evaluation, we apply ICD and DAMP concepts to silica cytotoxicity, providing new insights on the mechanisms driving the progress and/or the exacerbation of certain SiO2–related pathologies. Finally, by proposing self-DNA as new crucial DAMP, we aim to pave the way for the development of innovative and easy-to-perform predictive tests to better identify the hazard of fine and ultrafine silica particles. Importantly, such mechanisms could be extended to nano/micro plastics and diesel particles, providing strategic advice and reports on their health issues.

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Section: The "Previous" Model Elucidating the Proinflammatory Activit...mentioning

confidence: 99%

Think Beyond Particle Cytotoxicity: When Self-Cellular Components Released After Immunogenic Cell Death Explain Chronic Disease Development

Leinardi

Sanchez-Calero²,

Huaux³

2022

Front. Toxicol.

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“…Both IL-28 and STING results will be pursued in follow-up investigations. We previously addressed the role of STING-dependent self-DNA sensing in other models of lung inflammation and fibrosis ( 15 , 26 – 28 ). We also previously generated mice with AT1 cell-specific deletion of MyD88 using Aqp5 CRE , which showed a major reduction of papain-induced acute lung inflammation ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Lung inflammation and interstitial fibrosis by targeted alveolar epithelial type I cell death

Carignon,

De Moura Rodrigues,

Gosset

et al. 2023

Front. Immunol.

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IntroductionThe pathogenesis of chronic lung diseases is multifaceted with a major role of recurrent micro-injuries of the epithelium. While several reports clearly indicated a prominent role for surfactant-producing alveolar epithelial type 2 (AT2) cells, the contribution of gas exchange-permissive alveolar epithelial type 1 (AT1) cells has not been addressed yet. Here, we investigated whether repeated injury of AT1 cells leads to inflammation and interstitial fibrosis.MethodsWe chose an inducible model of AT1 cell depletion following local diphtheria toxin (DT) administration using an iDTR flox/flox (idTRfl/fl) X Aquaporin 5CRE (Aqp5CRE) transgenic mouse strain.ResultsWe investigated repeated doses and intervals of DT to induce cell death of AT1 cells causing inflammation and interstitial fibrosis. We found that repeated DT administrations at 1ng in iDTRfl/fl X Aqp5CRE mice cause AT1 cell death leading to inflammation, increased tissue repair markers and interstitial pulmonary fibrosis.DiscussionTogether, we demonstrate that depletion of AT1 cells using repeated injury represents a novel approach to investigate chronic lung inflammatory diseases and to identify new therapeutic targets.

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“…We thank Quesniaux and her colleagues for their commentary 1 regarding our article “Silica‐related diseases in the modern world.” 2 We wholeheartedly agree with their sentiment that understanding mechanisms of disease at the cellular and molecular level, rather than at the “macro” level, will lead to more effective therapies. This principle applies just as well to newly emerging diseases such as COVID‐19, as it does to ancient conditions such as silicosis.…”

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confidence: 99%

Reply to correspondence: Silica‐related diseases in the modern world: A role for self‐DNA sensing in lung inflammatory

Chambers

Hoy

2020

Allergy

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Silica‐related diseases in the modern world: A role for self‐DNA sensing in lung inflammatory diseases

Cited by 4 publications

References 6 publications

Think Beyond Particle Cytotoxicity: When Self-Cellular Components Released After Immunogenic Cell Death Explain Chronic Disease Development

Think Beyond Particle Cytotoxicity: When Self-Cellular Components Released After Immunogenic Cell Death Explain Chronic Disease Development

Lung inflammation and interstitial fibrosis by targeted alveolar epithelial type I cell death

Reply to correspondence: Silica‐related diseases in the modern world: A role for self‐DNA sensing in lung inflammatory

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