ArticlePloS one2014
Uncoupling between inflammatory and fibrotic responses to silica: evidence from MyD88 knockout mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Dietary docosahexaenoic acid supplementation inhibits acute pulmonary transcriptional and autoantibody responses to a single crystalline silica exposure in lupus-prone mice.Frontiers in immunology · 2024Article
- Environmental Causes of Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Cigarette Smoke-Induced Respiratory Response: Insights into Cellular Processes and Biomarkers.Antioxidants (Basel, Switzerland) · 2023Review
- Pulmonary Toxicity of Silica Linked to Its Micro- or Nanometric Particle Size and Crystal Structure: A Review.Nanomaterials (Basel, Switzerland) · 2022Review
- Think Beyond Particle Cytotoxicity: When Self-Cellular Components Released After Immunogenic Cell Death Explain Chronic Disease Development.Frontiers in toxicology · 2022Review
- Rapid Induction of Pulmonary Inflammation, Autoimmune Gene Expression, and Ectopic Lymphoid Neogenesis Following Acute Silica Exposure in Lupus-Prone Mice.Frontiers in immunology · 2021Article
- Interpreting Immunoregulation in Lung Fibrosis: A New Branch of the Immune Model.Frontiers in immunology · 2021Review
- Pulmonary toxicants and fibrosis: innate and adaptive immune mechanisms.Toxicology and applied pharmacology · 2020Review
- MyD88 regulates a prolonged adaptation response to environmental dust exposure-induced lung disease.Respiratory research · 2020Article
- Inflammation via myeloid differentiation primary response gene 88 signaling mediates the fibrotic response to implantable synthetic poly(ethylene glycol) hydrogels.Acta biomaterialia · 2019Article
- Loss of myeloid-specific protein phosphatase 2A enhances lung injury and fibrosis and results in IL-10-dependent sensitization of epithelial cell apoptosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Immediate Release of Gastrin-Releasing Peptide Mediates Delayed Radiation-Induced Pulmonary Fibrosis.The American journal of pathology · 2019Article
- Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2019Review
- Aggregated Tau activates NLRP3-ASC inflammasome exacerbating exogenously seeded and non-exogenously seeded Tau pathology in vivo.Acta neuropathologica · 2019Article
- Comparative cytotoxicity of respirable surface-treated/untreated calcium carbonate rock dust particles in vitro.Toxicology and applied pharmacology · 2019Article
- Emerging Role of Immunosuppression in Diseases Induced by Micro- and Nano-Particles: Time to Revisit the Exclusive Inflammatory Scenario.Frontiers in immunology · 2018Review
- Regulation of TLR4 in silica-induced inflammation: An underlying mechanism of silicosis.International journal of medical sciences · 2018Article
- Macrophage Recognition of Crystals and Nanoparticles.Frontiers in immunology · 2018Review
- Myeloid differentiation primary response gene (MyD) 88 signalling is not essential for intestinal fibrosis development.Scientific reports · 2017Article
- Stat-6 signaling pathway and not Interleukin-1 mediates multi-walled carbon nanotube-induced lung fibrosis in mice: insights from an adverse outcome pathway framework.Particle and fibre toxicology · 2017Article
Corrections and comments
- Erratum issuedGiordano, Giulia [added]
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The exact implication of innate immunity in granuloma formation and irreversible lung fibrosis remains to be determined. In this study, we examined the lung inflammatory and fibrotic responses to silica in MyD88-knockout (KO) mice. In comparison to wild-type (WT) mice, we found that MyD88-KO animals developed attenuated lung inflammation, neutrophil accumulation and IL-1β release in response to silica. Granuloma formation was also less pronounced in MyD88-KO mice after silica. This limited inflammatory response was not accompanied by a concomitant attenuation of lung collagen accumulation after silica. Histological analyses revealed that while pulmonary fibrosis was localized in granulomas in WT animals, it was diffusely distributed throughout the parenchyma in MyD88-KO mice. Robust collagen accumulation was also observed in mice KO for several other components of innate immunity (IL-1R, IL-1, ASC, NALP3, IL-18R, IL-33R, TRIF, and TLR2-3-4,). We additionally show that pulmonary fibrosis in MyD88-KO mice was associated with the accumulation of pro-fibrotic regulatory T lymphocytes (T regs) and pro-fibrotic cytokine expression (TGF-β, IL-10 and PDGF-B), not with T helper (Th) 17 cell influx. Our findings indicate that the activation of MyD88-related innate immunity is central in the establishment of particle-induced lung inflammatory and granuloma responses. The development of lung fibrosis appears uncoupled from inflammation and may be orchestrated by a T reg-associated pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.