ArticleACS nano2014
Graphene oxide attenuates Th2-type immune responses, but augments airway remodeling and hyperresponsiveness in a murine model of asthma.
Article in ACS nano, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 62 citations in OpenAlex.
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- Toxicity and Mechanisms of Engineered Nanoparticles in Animals with Established Allergic Asthma.International journal of nanomedicine · 2023Review
- Recent applications of immunomodulatory biomaterials for disease immunotherapy.Exploration (Beijing, China) · 2022Review
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- Immunotoxicity of Carbon-Based Nanomaterials, Starring Phagocytes.International journal of molecular sciences · 2022Review
- Biomarkers of nanomaterials hazard from multi-layer data.Nature communications · 2022Article
- Concepts of advanced therapeutic delivery systems for the management of remodeling and inflammation in airway diseases.Future medicinal chemistry · 2022Review
- Regulatory T Cells: Angels or Demons in the Pathophysiology of Sepsis?Frontiers in immunology · 2022Review
- CHI3L1 in the CSF is a potential biomarker for anti-leucine-rich glioma inactivated 1 encephalitis.Frontiers in immunology · 2022Article
- Size-Dependent Pulmonary Impact of Thin Graphene Oxide Sheets in Mice: Toward Safe-by-Design.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Toxicology data of graphene-family nanomaterials: an update.Archives of toxicology · 2020Review
- YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway.Cell cycle (Georgetown, Tex.) · 2020Article
- Surface area- and mass-based comparison of fine and ultrafine nickel oxide lung toxicity and augmentation of allergic response in an ovalbumin asthma model.Inhalation toxicology · 2019Article
- Graphene oxide polarizes iNKT cells for production of TGFβ and attenuates inflammation in an iNKT cell-mediated sepsis model.Scientific reports · 2018Article
- The Toxicology of Engineered Nanomaterials in Asthma.Current environmental health reports · 2018Review
- Mechanistic insight into the impact of nanomaterials on asthma and allergic airway disease.Particle and fibre toxicology · 2017Review
- Ins and Outs in Environmental and Occupational Safety Studies of Asthma and Engineered Nanomaterials.ACS nano · 2017Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Several lines of evidence indicate that exposure to nanoparticles (NPs) is able to modify airway immune responses, thus facilitating the development of respiratory diseases. Graphene oxide (GO) is a promising carbonaceous nanomaterial with unique physicochemical properties, envisioned for a multitude of medical and industrial applications. In this paper, we determined how exposure to GO modulates the allergic pulmonary response. Using a murine model of ovalbumin (OVA)-induced asthma, we revealed that GO, given at the sensitization stage, augmented airway hyperresponsiveness and airway remodeling in the form of goblet cell hyperplasia and smooth muscle hypertrophy. At the same time, the levels of the cytokines IL-4, IL-5, and IL-13 were reduced in broncho-alveolar lavage (BAL) fluid in GO-exposed mice. Exposure to GO during sensitization with OVA decreased eosinophil accumulation and increased recruitment of macrophages in BAL fluid. In line with the cytokine profiles, sensitization with OVA in the presence of GO stimulated the production of OVA-specific IgG2a and down-regulated the levels of IgE and IgG1. Moreover, exposure to GO increased the macrophage production of the mammalian chitinases, CHI3L1 and AMCase, whose expression is associated with asthma. Finally, molecular modeling has suggested that GO may directly interact with chitinase, affecting AMCase activity, which has been directly proven in our studies. Thus, these data show that GO exposure attenuates Th2 immune response in a model of OVA-induced asthma, but leads to potentiation of airway remodeling and hyperresponsiveness, with the induction of mammalian chitinases.
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Registered trials
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.