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Molecular Mechanism of Lung Injury Caused by Environmental Factors
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Molecular Mechanism of Lung Injury Caused by Environmental Factors

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

Deadline for manuscript submissions: closed (25 February 2024) | Viewed by 12768

Special Issue Editors

Dr. Maria Lisa Garavaglia

E-Mail Website
Guest Editor
Department of Biosciences, University of Milan, 20122 Milan, Italy
Interests: cigarette smoke; cellular oxidative stress; inflammation; smoking related diseases; antioxidant
Special Issues, Collections and Topics in MDPI journals
Dr. Francesca Bodega

E-Mail Website
Guest Editor
Department of Pathophysiology and Transplantation, University of Milan, 20122 Milano, MI, Italy
Interests: pleural liquid; pleural friction; alveolar cells; mesothelial cells; mesothelial transport
Dr. Cristina Porta

E-Mail Website
Guest Editor
Department of Pathophysiology and Transplantation, University of Milan, 20122 Milano, MI, Italy
Interests: epithelial and mesothelial barriers; fluid, ion and polypeptide transports; MALT; pleural liquid; pleural friction

Special Issue Information

Dear Colleagues,

The lungs are among the most important target of the harmful effects of environmental agents due to their large exchange surface, with the presence of a thin epithelial sheet to separate the internal environment from the external one.

The environmental factors that can affect lung function can be physical (for example, ionizing radiation such as radon) or chemical, such as asbestos, dioxins, metals (e.g., chromium, arsenic, nickel, cobalt, etc.) and other pollutants present in industrial and domestic emissions or in smoking—both active and passive. Although many countries have guidelines and policies for the prevention and control of these risk factors, the "environmental challenge" is still current and far from being resolved.

Environmental pollutants can have short- and long-term effects on lung health and be related to the development of diseases—such as COPD, asthma, and cancer, to name a few—which undermine people's well-being, health or even life.

Knowledge of the molecular mechanisms put in place by the specific environmental factors allows us to create a precise picture of their mechanisms of action, tailoring direct and prompt interventional approaches to address the driving mechanisms leading to the development of lung diseases.

This Special Issue focuses on the molecular functional modifications induced by environmental factors on the lungs.

We welcome your contributions, original papers, or review articles, on the cellular or molecular pathological changes induced by environmental factors, in acute or chronic form, in the lungs, as well as on new possible approaches to handle these damages.

Dr. Maria Lisa Garavaglia
Dr. Francesca Bodega
Dr. Cristina Porta
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • environment
  • pollutants
  • respiratory system
  • lung injury
  • epithelial–mesenchymal transition
  • oxidative stress
  • inflammation
  • surfactant
  • epithelial lining fluid
  • alveolar barrier pathology

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Published Papers (5 papers)

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Research

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11 pages, 3415 KiB  
Article
Effects of Radioactive 56MnO2 Particle Inhalation on Mouse Lungs: A Comparison between C57BL and BALB/c
by Zhaslan Abishev, Bakhyt Ruslanova, Saulesh Apbassova, Dariya Shabdarbayeva, Nailya Chaizhunussova, Altai Dyusupov, Almas Azhimkhanov, Kassym Zhumadilov, Valeriy Stepanenko, Sergey Ivanov, Peter Shegay, Andrey Kaprin, Masaharu Hoshi and Nariaki Fujimoto
Int. J. Mol. Sci. 2023, 24(24), 17605; https://doi.org/10.3390/ijms242417605 - 18 Dec 2023
Cited by 1 | Viewed by 1081
Abstract
The effects of residual radiation from atomic bombs have been considered to be minimal because of its low levels of external radioactivity. However, studies involving atomic bomb survivors exposed to only residual radiation in Hiroshima and Nagasaki have indicated possible adverse health effects. [...] Read more.
The effects of residual radiation from atomic bombs have been considered to be minimal because of its low levels of external radioactivity. However, studies involving atomic bomb survivors exposed to only residual radiation in Hiroshima and Nagasaki have indicated possible adverse health effects. Thus, we investigated the biological effects of radioactive dust of manganese dioxide 56 (56MnO2), a major radioisotope formed in soil by neutron beams from a bomb. Previously, we investigated C57BL mice exposed to 56MnO2 and found pulmonary gene expression changes despite low radiation doses. In this study, we examined the effects in a radiation-sensitive strain of mice, BALB/c, and compared them with those in C57BL mice. The animals were exposed to 56MnO2 particles at two radioactivity levels and examined 3 and 65 days after exposure. The mRNA expression of pulmonary pathophysiology markers, including Aqp1, Aqp5, and Smad7, and radiation-sensitive genes, including Bax, Phlda3, and Faim3, was determined in the lungs. The radiation doses absorbed in the lungs ranged from 110 to 380 mGy; no significant difference was observed between the two strains. No exposure-related pathological changes were observed in the lungs of any group. However, the mRNA expression of Aqp1 was significantly elevated in C57BL mice but not in BALB/c mice 65 days after exposure, whereas no changes were observed in external γ-rays (2 Gy) in either strain. In contrast, Faim3, a radiation-dependently downregulated gene, was reduced by 56MnO2 exposure in BALB/c mice but not in C57BL mice. These data demonstrate that inhalation exposure to 56MnO2 affected the expression of pulmonary genes at doses <380 mGy, which is comparable to 2 Gy of external γ-irradiation, whereas the responses differed between the two mouse strains. Full article
(This article belongs to the Special Issue Molecular Mechanism of Lung Injury Caused by Environmental Factors)
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14 pages, 2719 KiB  
Article
Transcriptomic Profiling the Effects of Airway Exposure of Zinc Oxide and Silver Nanoparticles in Mouse Lungs
by Lan Zhao, Shuyuan Wang, Marit Ilves, Sanna Lehtonen, Leena Saikko, Hani El-Nezami, Harri Alenius and Piia Karisola
Int. J. Mol. Sci. 2023, 24(6), 5183; https://doi.org/10.3390/ijms24065183 - 8 Mar 2023
Cited by 1 | Viewed by 1903
Abstract
Consumers and manufacturers are exposed to nanosized zinc oxide (nZnO) and silver particles (nAg) via airways, but their biological effects are still not fully elucidated. To understand the immune effects, we exposed mice to 2, 10, or 50 μg of nZnO or nAg [...] Read more.
Consumers and manufacturers are exposed to nanosized zinc oxide (nZnO) and silver particles (nAg) via airways, but their biological effects are still not fully elucidated. To understand the immune effects, we exposed mice to 2, 10, or 50 μg of nZnO or nAg by oropharyngeal aspiration and analyzed the global gene expression profiles and immunopathological changes in the lungs after 1, 7, or 28 days. Our results show that the kinetics of responses varied in the lungs. Exposure to nZnO resulted in the highest accumulation of F4/80- and CD3-positive cells, and the largest number of differentially expressed genes (DEGs) were identified after day 1, while exposure to nAg caused peak responses at day 7. Additionally, nZnO mainly activated the innate immune responses leading to acute inflammation, whereas the nAg activated both innate and adaptive immune pathways, with long-lasting effects. This kinetic-profiling study provides an important data source to understand the cellular and molecular processes underlying nZnO- and nAg-induced transcriptomic changes, which lead to the characterization of the corresponding biological and toxicological effects of nZnO and nAg in the lungs. These findings could improve science-based hazard and risk assessment and the development of safe applications of engineered nanomaterials (ENMs), e.g., in biomedical applications. Full article
(This article belongs to the Special Issue Molecular Mechanism of Lung Injury Caused by Environmental Factors)
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Review

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15 pages, 1127 KiB  
Review
Environmental Causes of Idiopathic Pulmonary Fibrosis
by Sheiphali Gandhi, Roberto Tonelli, Margaret Murray, Anna Valeria Samarelli and Paolo Spagnolo
Int. J. Mol. Sci. 2023, 24(22), 16481; https://doi.org/10.3390/ijms242216481 - 18 Nov 2023
Cited by 8 | Viewed by 3086
Abstract
Idiopathic pulmonary fibrosis (IPF), the most common and severe of the idiopathic interstitial pneumonias, is a chronic and relentlessly progressive disease, which occurs mostly in middle-aged and elderly males. Although IPF is by definition “idiopathic”, multiple factors have been reported to increase disease [...] Read more.
Idiopathic pulmonary fibrosis (IPF), the most common and severe of the idiopathic interstitial pneumonias, is a chronic and relentlessly progressive disease, which occurs mostly in middle-aged and elderly males. Although IPF is by definition “idiopathic”, multiple factors have been reported to increase disease risk, aging being the most prominent one. Several occupational and environmental exposures, including metal dust, wood dust and air pollution, as well as various lifestyle variables, including smoking and diet, have also been associated with an increased risk of IPF, probably through interaction with genetic factors. Many of the predisposing factors appear to act also as trigger for acute exacerbations of the disease, which herald a poor prognosis. The more recent literature on inhalation injuries has focused on the first responders in the World Trade Center attacks and military exposure. In this review, we present an overview of the environmental and occupational causes of IPF and its pathogenesis. While our list is not comprehensive, we have selected specific exposures to highlight based on their overall disease burden. Full article
(This article belongs to the Special Issue Molecular Mechanism of Lung Injury Caused by Environmental Factors)
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17 pages, 4080 KiB  
Review
Asbestos and Iron
by Andrew J. Ghio, Matthew Stewart, Rahul G. Sangani, Elizabeth N. Pavlisko and Victor L. Roggli
Int. J. Mol. Sci. 2023, 24(15), 12390; https://doi.org/10.3390/ijms241512390 - 3 Aug 2023
Cited by 2 | Viewed by 2729
Abstract
Theories of disease pathogenesis following asbestos exposure have focused on the participation of iron. After exposure, an open network of negatively charged functional groups on the fiber surface complexes host metals with a preference for iron. Competition for iron between the host and [...] Read more.
Theories of disease pathogenesis following asbestos exposure have focused on the participation of iron. After exposure, an open network of negatively charged functional groups on the fiber surface complexes host metals with a preference for iron. Competition for iron between the host and the asbestos results in a functional metal deficiency. The homeostasis of iron in the host is modified by the cell response, including increased import to correct the loss of the metal to the fiber surface. The biological effects of asbestos develop in response to and are associated with the disruption of iron homeostasis. Cell iron deficiency in the host following fiber exposure activates kinases and transcription factors, which are associated with the release of mediators coordinating both inflammatory and fibrotic responses. Relative to serpentine chrysotile, the clearance of amphiboles is incomplete, resulting in translocation to the mesothelial surface of the pleura. Since the biological effect of asbestos is dependent on retention of the fiber, the sequestration of iron by the surface, and functional iron deficiency in the cell, the greater clearance (i.e., decreased persistence) of chrysotile results in its diminished impact. An inability to clear asbestos from the lower respiratory tract initiates a host process of iron biomineralization (i.e., asbestos body formation). Host cells attempt to mobilize the metal sequestered by the fiber surface by producing superoxide at the phagosome membrane. The subsequent ferrous cation is oxidized and undergoes hydrolysis, creating poorly crystalline iron oxyhydroxide (i.e., ferrihydrite) included in the coat of the asbestos body. Full article
(This article belongs to the Special Issue Molecular Mechanism of Lung Injury Caused by Environmental Factors)
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32 pages, 3543 KiB  
Review
Molecular Impact of Conventional and Electronic Cigarettes on Pulmonary Surfactant
by Maria Lisa Garavaglia, Francesca Bodega, Cristina Porta, Aldo Milzani, Chiara Sironi and Isabella Dalle-Donne
Int. J. Mol. Sci. 2023, 24(14), 11702; https://doi.org/10.3390/ijms241411702 - 20 Jul 2023
Cited by 2 | Viewed by 2923
Abstract
The alveolar epithelium is covered by a non-cellular layer consisting of an aqueous hypophase topped by pulmonary surfactant, a lipo-protein mixture with surface-active properties. Exposure to cigarette smoke (CS) affects lung physiology and is linked to the development of several diseases. The macroscopic [...] Read more.
The alveolar epithelium is covered by a non-cellular layer consisting of an aqueous hypophase topped by pulmonary surfactant, a lipo-protein mixture with surface-active properties. Exposure to cigarette smoke (CS) affects lung physiology and is linked to the development of several diseases. The macroscopic effects of CS are determined by several types of cell and molecular dysfunction, which, among other consequences, lead to surfactant alterations. The purpose of this review is to summarize the published studies aimed at uncovering the effects of CS on both the lipid and protein constituents of surfactant, discussing the molecular mechanisms involved in surfactant homeostasis that are altered by CS. Although surfactant homeostasis has been the topic of several studies and some molecular pathways can be deduced from an analysis of the literature, it remains evident that many aspects of the mechanisms of action of CS on surfactant homeostasis deserve further investigation. Full article
(This article belongs to the Special Issue Molecular Mechanism of Lung Injury Caused by Environmental Factors)
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