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Molecular Mechanisms of Major Inflammatory Occupational Diseases

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

Deadline for manuscript submissions: closed (30 March 2022) | Viewed by 17598

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Special Issue Editor

Prof. Dr. Shanbeh Zienolddiny

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Guest Editor

National Institute of Occupational Health, 0033 Oslo, Norway
Interests: occupational health; inflammation; molecular genetics; carcinogenesis

Special Issue Information

Dear Colleagues,

Occupational exposure to chemicals and biological agents is common in many work places. Depending on the type of chemical or biological agent, they may lead to adverse health effects in the workers who are handling these agents through the manufacturing, processing, use, or waste handling. Health effects may vary and could include cardiovascular, pulmonary (i.e., COPD, fibrosis, etc.), neurodegenerative diseases, and cancer. However, molecular and cellular mechanisms are unknown but inflammation is a putative common mechanism that operates in these diseases. Knowing mechanisms of disease will help in identification of molecular markers that could be used for prevention and in particular for design of personalized prevention strategies. Molecular and cellular markers of disease are of utmost importance for personalized prevention as these markers are important for personalized diagnostic and treatment strategies. In this Special Issue, the focus will be on the cellular and molecular markers that drive acute inflammation to become chronic inflammtion and so leading to development of inflammatory occupational diseases.

Prof. Dr. Shanbeh Zienolddiny
Guest Editor

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

occupational health
inflammation
CVD
COPD
fibrosis

Published Papers (5 papers)

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Research

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16 pages, 1431 KiB

Open AccessArticle

Multiwalled Carbon Nanotubes Induce Fibrosis and Telomere Length Alterations

by Mayes Alswady-Hoff, Johanna Samulin Erdem, Mona Aleksandersen, Kristine Haugen Anmarkrud, Øivind Skare, Fang-Chin Lin, Vincent Simensen, Yke Jildouw Arnoldussen, Vidar Skaug, Erik Ropstad and Shanbeh Zienolddiny-Narui

Int. J. Mol. Sci. 2022, 23(11), 6005; https://doi.org/10.3390/ijms23116005 - 26 May 2022

Cited by 5 | Viewed by 1711

Abstract

Telomere shortening can result in cellular senescence and in increased level of genome instability, which are key events in numerous of cancer types. Despite this, few studies have focused on the effect of nanomaterial exposure on telomere length as a possible mechanism involved in nanomaterial-induced carcinogenesis. In this study, effects of exposure to multiwalled carbon nanotubes (MWCNT) on telomere length were investigated in mice exposed by intrapleural injection, as well as in human lung epithelial and mesothelial cell lines. In addition, cell cycle, apoptosis, and regulation of genes involved in DNA damage repair were assessed. Exposure to MWCNT led to severe fibrosis, infiltration of inflammatory cells in pleura, and mesothelial cell hyperplasia. These histological alterations were accompanied by deregulation of genes involved in fibrosis and immune cell recruitment, as well as a significant shortening of telomeres in the pleura and the lung. Assessment of key carcinogenic mechanisms in vitro confirmed that long-term exposure to the long MWCNT led to a prominent telomere shortening in epithelial cells, which coincided with G1-phase arrest and enhanced apoptosis. Altogether, our data show that telomere shortening resulting in cell cycle arrest and apoptosis may be an important mechanism in long MWCNT-induced inflammation and fibrosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Major Inflammatory Occupational Diseases)

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13 pages, 9584 KiB

Open AccessArticle

Oxamate Attenuates Glycolysis and ER Stress in Silicotic Mice

by Na Mao, Yuhang Fan, Wenjing Liu, Honghao Yang, Yi Yang, Yaqian Li, Fuyu Jin, Tian Li, Xinyu Yang, Xuemin Gao, Wenchen Cai, Heliang Liu, Hong Xu, Shifeng Li and Fang Yang

Int. J. Mol. Sci. 2022, 23(6), 3013; https://doi.org/10.3390/ijms23063013 - 10 Mar 2022

Cited by 6 | Viewed by 2633

Abstract

Glycolysis and ER stress have been considered important drivers of pulmonary fibrosis. However, it is not clear whether glycolysis and ER stress are interconnected and if those interconnections regulate the development of pulmonary fibrosis. Our previous studies found that the expression of LDHA, a key enzyme involved in glycolysis, was increased in silica-induced macrophages and silicotic models, and it was closely related to silicosis fibrosis by participating in inflammatory response. However, whether pharmacological inhibition of LDHA is beneficial to the amelioration of silicosis fibrosis remains unclear. In this study, we investigated the effects of oxamate, a potent inhibitor of LDHA, on the regulation of glycolysis and ER stress in alveolar macrophages and silicotic mice. We found that silica induced the upregulation of glycolysis and the expression of key enzymes directly involved in ER stress in NR8383 macrophages. However, treatment of the macrophages and silicotic mice with oxamate attenuated glycolysis and ER stress by inhibiting LDHA, causing a decrease in the production of lactate. Therefore, oxamate demonstrated an anti-fibrotic role by reducing glycolysis and ER stress in silicotic mice. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Major Inflammatory Occupational Diseases)

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14 pages, 7133 KiB

Open AccessArticle

Glycolytic Reprogramming in Silica-Induced Lung Macrophages and Silicosis Reversed by Ac-SDKP Treatment

by Na Mao, Honghao Yang, Jie Yin, Yaqian Li, Fuyu Jin, Tian Li, Xinyu Yang, Ying Sun, Heliang Liu, Hong Xu and Fang Yang

Int. J. Mol. Sci. 2021, 22(18), 10063; https://doi.org/10.3390/ijms221810063 - 17 Sep 2021

Cited by 17 | Viewed by 3371

Abstract

Glycolytic reprogramming is an important metabolic feature in the development of pulmonary fibrosis. However, the specific mechanism of glycolysis in silicosis is still not clear. In this study, silicotic models and silica-induced macrophage were used to elucidate the mechanism of glycolysis induced by silica. Expression levels of the key enzymes in glycolysis and macrophage activation indicators were analyzed by Western blot, qRT-PCR, IHC, and IF analyses, and by using a lactate assay kit. We found that silica promotes the expression of the key glycolysis enzymes HK2, PKM2, LDHA, and macrophage activation factors iNOS, TNF-α, Arg-1, IL-10, and MCP1 in silicotic rats and silica-induced NR8383 macrophages. The enhancement of glycolysis and macrophage activation induced by silica was reduced by Ac-SDKP or siRNA-Ldha treatment. This study suggests that Ac-SDKP treatment can inhibit glycolytic reprogramming in silica-induced lung macrophages and silicosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Major Inflammatory Occupational Diseases)

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Review

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47 pages, 4228 KiB

Open AccessReview

Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants

by Dhruba Pathak and Krishnan Sriram

Int. J. Mol. Sci. 2023, 24(3), 2272; https://doi.org/10.3390/ijms24032272 - 23 Jan 2023

Cited by 19 | Viewed by 3330

Abstract

Occupational injuries and toxicant exposures lead to the development of neuroinflammation by activating distinct mechanistic signaling cascades that ultimately culminate in the disruption of neuronal function leading to neurological and neurodegenerative disorders. The entry of toxicants into the brain causes the subsequent activation of glial cells, a response known as ‘reactive gliosis’. Reactive glial cells secrete a wide variety of signaling molecules in response to neuronal perturbations and thus play a crucial role in the progression and regulation of central nervous system (CNS) injury. In parallel, the roles of protein phosphorylation and cell signaling in eliciting neuroinflammation are evolving. However, there is limited understanding of the molecular underpinnings associated with toxicant- or occupational injury-mediated neuroinflammation, gliosis, and neurological outcomes. The activation of signaling molecules has biological significance, including the promotion or inhibition of disease mechanisms. Nevertheless, the regulatory mechanisms of synergism or antagonism among intracellular signaling pathways remain elusive. This review highlights the research focusing on the direct interaction between the immune system and the toxicant- or occupational injury-induced gliosis. Specifically, the role of occupational injuries, e.g., trips, slips, and falls resulting in traumatic brain injury, and occupational toxicants, e.g., volatile organic compounds, metals, and nanoparticles/nanomaterials in the development of neuroinflammation and neurological or neurodegenerative diseases are highlighted. Further, this review recapitulates the recent advancement related to the characterization of the molecular mechanisms comprising protein phosphorylation and cell signaling, culminating in neuroinflammation. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Major Inflammatory Occupational Diseases)

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19 pages, 1346 KiB

Open AccessReview

Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge

by Wiwin Is Effendi and Tatsuya Nagano

Int. J. Mol. Sci. 2022, 23(11), 6064; https://doi.org/10.3390/ijms23116064 - 28 May 2022

Cited by 26 | Viewed by 5754

Abstract

CTGF is upregulated in patients with idiopathic pulmonary fibrosis (IPF), characterized by the deposition of a pathological extracellular matrix (ECM). Additionally, many omics studies confirmed that aberrant cellular senescence-associated mitochondria dysfunction and metabolic reprogramming had been identified in different IPF lung cells (alveolar epithelial cells, alveolar endothelial cells, fibroblasts, and macrophages). Here, we reviewed the role of the CTGF in IPF lung cells to mediate anomalous senescence-related metabolic mechanisms that support the fibrotic environment in IPF. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Major Inflammatory Occupational Diseases)

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