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Chemical and Atmospheric Research in Toxicology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 4572

Special Issue Editor


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Guest Editor
Department of Nursing, University of Shizuoka, Shizuoka 422-8526, Japan
Interests: chemicals; PM2.5; allergy; respiratory medicine; PAH
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, “Chemical and Atmospheric Research in Toxicology”, will cover a selection of recent research topics and review articles related to the environmental toxicology. Up-to-date review articles, commentaries, and both epidemiologic and experimental papers are all welcome.

In particular, this issue focuses on environmental pollution regarding chemicals and airborne particulate matters (PM). Some kinds of environmental chemicals have been discussed to serve as “endocrine disruptors” other than carcinogens. Further, recent research has proven that some chemical substances adversely activate immune systems and exacerbate immune-related disorders, including allergies and collagen vascular diseases. More recently, advanced studies have suggested that several chemicals alter metabolism and/or adipogenesis, resulting in diabetes, non-alcoholic fatty liver disease, and obesity. Among them, nonmonotonic dose–response curves are observed; thus, further studies are required to reconsider toxicological no-observed-adverse-effect level. On the other hand, air pollution including PM induces/aggravates several types of airway diseases. Furthermore, researchers in environmental sciences have been interested in the correlation between toxicity and smaller particles (defined as “nanoparticles/nanomaterials”). Other causal characterization of particles in terms of chemical/metal composition, shape, and surface charge are aggressively studied as well.

Dr. Ken-ichiro Inoue
Guest Editor

Manuscript Submission Information

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Keywords

  • particulate matters
  • endocrine disrupting chemicals
  • air pollution
  • nanoparticles
  • nanomaterials
  • carcinogenesis/mutagenesis
  • maternal exposure
  • allergy

Published Papers (1 paper)

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Research

17 pages, 3973 KiB  
Article
Particulate Matter Increases the Severity of Bleomycin-Induced Pulmonary Fibrosis through KC-Mediated Neutrophil Chemotaxis
by I-Yin Cheng, Chen-Chi Liu, Jiun-Han Lin, Tien-Wei Hsu, Jyuan-Wei Hsu, Anna Fen-Yau Li, Wen-Chao Ho, Shih-Chieh Hung and Han-Shui Hsu
Int. J. Mol. Sci. 2020, 21(1), 227; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21010227 - 28 Dec 2019
Cited by 11 | Viewed by 4160
Abstract
Background: Although particular matter (PM) increases incidence and severity of idiopathic pulmonary fibrosis, the underlying mechanism remains elusive. Methods: The effects of PM were evaluated in a murine model of bleomycin-induced pulmonary fibrosis. Mice were divided into four groups, receiving: (1) Saline (control), [...] Read more.
Background: Although particular matter (PM) increases incidence and severity of idiopathic pulmonary fibrosis, the underlying mechanism remains elusive. Methods: The effects of PM were evaluated in a murine model of bleomycin-induced pulmonary fibrosis. Mice were divided into four groups, receiving: (1) Saline (control), (2) bleomycin, (3) PM, or (4) bleomycin plus PM (Bleo+PM). Additional groups of Bleo+PM mice were treated with sivelestat (an inhibitor of neutrophil elastase) or reparixin (a C-X-C motif chemokine receptor 2 antagonist), or were genetically modified with keratinocyte chemoattractant (KC) deletion. Results: Pulmonary fibrosis was not observed in the control or PM groups. Bleomycin induced pulmonary fibrosis within 14 days. The Bleo+PM group showed worse pulmonary fibrosis when compared to the bleomycin group. Analyses of immune cell profile and chemokine/cytokine concentrations at day 2-bronchoalveolar lavage fluid (BALF) revealed that the Bleo+PM group had increased neutrophil number and elastase level and KC concentration compared to the bleomycin group. Neutrophil elastase activated the Smad2/Smad3/α-SMA pathway to induce collagen deposition, while sivelestat abrogated the increased severity of pulmonary fibrosis caused by PM. Chemotaxis assay revealed that BALF of the Bleo+PM group recruited neutrophil, which was dependent on KC. Further, genetic KC deletion or pharmaceutical inhibition of KC binding to CXCR2 with reparixin ameliorated the PM-induced increased severity of pulmonary fibrosis. Conclusions: These data provide evidence that the PM-induced increased severity of pulmonary fibrosis depends on KC-mediated neutrophil chemotaxis and give additional mechanic insight that will aid in the development of therapeutic strategies. Full article
(This article belongs to the Special Issue Chemical and Atmospheric Research in Toxicology)
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