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Molecular Pathophysiology of Chronic Lung Disease

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 22661

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Special Issue Editors

Prof. Dr. Hsiao-Chi Chuang

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Guest Editor

School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
Interests: inhalation toxicology; environmental medicine; occupational medicine
Special Issues, Collections and Topics in MDPI journals

Dr. Chia-Li Han

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Guest Editor

Master Program for Clinical Pharmacogenomics and Pharmacoproteomics, College of Pharmacy, Taipei Medical University, Taipei 110, Taiwan
Interests: biological mass spectrometry; membrane proteomics; biomarker discovery; proteogenomics

Dr. Yen-Chou Chen

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Guest Editor

Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
Interests: inflammation mechanism; anti-cancer drug action mechanism

Special Issue Information

Dear Colleagues,

Chronic lung disease may be caused by smoking tobacco or by breathing in secondhand tobacco smoke, chemical fumes, dust, or other forms of air pollution. Types of chronic lung disease include asthma, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, asbestosis, pneumonitis, and other lung conditions. Chronic lung diseases are not curable; however, various forms of treatment that help dilate major air passages and improve shortness of breath can help control symptoms and increase the quality of life for people with the disease.

Every piece of new information matters in the path from the unknown to translational research on chronic lung diseases. The objective of this Special Issue is to create a multidisciplinary forum for better understanding the molecular pathophysiology of chronic lung diseases, as well as the potential application to clinical therapy and diagnosis.

We welcome research of exceptional merit covering one or more of the following topics:

Molecular mechanisms of chronic lung disease;
Pathophysiology of chronic lung disease;
Biomarkers in chronic lung disease;
New drugs in chronic lung disease treatment.

Dr. Hsiao-Chi Chuang
Dr. Chia-Li Han
Dr. Yen-Chou Chen
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

asthma
biomarker
chronic obstructive pulmonary disease
pathology
pharmarcology
physiology
pulmonary fibrosis
respiratory
toxicology

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Published Papers (6 papers)

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Research

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10 pages, 1402 KiB

Open AccessArticle

Applicability of the MASK-Air^® App to Severe Asthma Treated with Biologic Molecules: A Pilot Study

by Alida Benfante, Bernardo Sousa-Pinto, Gianluca Pillitteri, Salvatore Battaglia, Joao Fonseca, Jean Bousquet and Nicola Scichilone

Int. J. Mol. Sci. 2022, 23(19), 11470; https://doi.org/10.3390/ijms231911470 - 29 Sep 2022

Cited by 7 | Viewed by 1906

Abstract

MASK-air^®, a good practice of the DG Santé, has been fully validated in allergic rhinitis, but little is known about its applicability to asthmatics. We explored whether the MASK-air^® application is applicable to patients with severe asthma. Severe asthmatics were proposed to use the MASK-air^® application for 6 months, along with best practice treatment. Treatment of the patients was not changed based on the application results. The evolution of the visual analogue scales (VAS) for asthma, shortness of breath, rhinitis, conjunctivitis, work, and sleep was monitored using MASK-air^®. Adherence to MASK-air^® and to the asthma treatment was also checked. Thirteen patients reported on 1229 days of MASK-air^® use. The average application adherence was 51.8% (range: 19.7–98.9%). There was no correlation between application and medication adherence. Highly variably trends were found for the VAS for asthma. Five patients had over 90% well-controlled days, four had well- or moderately controlled asthma (with up to 20% uncontrolled days), one patient had moderately controlled asthma with approximately 20% uncontrolled days, and one patient had 80% uncontrolled days. Highly significant correlations were found for the VAS for asthma, and other patients reported VASs for work, dyspnea, sleep, and rhinitis. MASK-air^® can be used in patients with severe asthma. VAS asthma appears to be an interesting patient-reported outcome highly correlated with dyspnea and impacts on work. Adherence to the application was better than that for rhinitis, but it needs to be improved. Full article

(This article belongs to the Special Issue Molecular Pathophysiology of Chronic Lung Disease)

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17 pages, 2469 KiB

Open AccessArticle

Home Dust Mites Promote MUC5AC Hyper-Expression by Modulating the sNASP/TRAF6 Axis in the Airway Epithelium

by Ming-Zhen Chen, Shao-An Wang, Shih-Chang Hsu, Kleiton Augusto Santos Silva and Feng-Ming Yang

Int. J. Mol. Sci. 2022, 23(16), 9405; https://doi.org/10.3390/ijms23169405 - 20 Aug 2022

Cited by 2 | Viewed by 2339

Abstract

House dust mites (HDMs) are a common source of respiratory allergens responsible for allergic asthma and innate immune responses in human diseases. Since HDMs are critical factors in the triggering of allergen-induced airway mucosa from allergic asthma, we aimed to investigate the mechanisms of Toll-like receptors (TLR) in the signaling of the HDM extract that is involved in mucus hypersecretion and airway inflammation through the engagement of innate immunity. Previously, we reported that the somatic nuclear autoantigenic sperm protein (sNASP)/tumor necrosis factor receptor-associated factor 6 (TRAF6) axis controls the initiation of TLRs to maintain the homeostasis of the innate immune response. The present study showed that the HDM extract stimulated the biogenesis of Mucin 5AC (MUC5AC) in bronchial epithelial cells via the TLR2/4 signaling pathway involving MyD88 and TRAF6. Specifically, sNASP binds to TRAF6 in unstimulated bronchial epithelial cells to prevent the activation of TRAF6-depenedent kinases. Upon on HDMs’ stimulation, sNASP is phosphorylated, leading to the activation of TRAF6 downstream of the p38 MAPK and NF-κB signaling pathways. Further, NASP-knockdown enhanced TRAF6 signaling and MUC5AC biogenesis. In the HDM-induced mouse asthma model, we found that the HDM extract promoted airway hyperresponsiveness (AHR), MUC5AC, and allergen-specific IgE production as well as IL-5 and IL-13 for recruiting inflammatory cells. Treatment with the PEP-NASP peptide, a selective TRAF6-blocking peptide, ameliorated HDM-induced asthma in mice. In conclusion, this study indicated that the sNASP/TRAF6 axis plays a regulatory role in asthma by modulating mucus overproduction, and the PEP-NASP peptide might be a potential target for asthma treatment. Full article

(This article belongs to the Special Issue Molecular Pathophysiology of Chronic Lung Disease)

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14 pages, 2692 KiB

Open AccessArticle

Reduction of Emphysema Severity by Human Umbilical Cord-Derived Mesenchymal Stem Cells in Mice

by Vincent Laiman, Yueh-Lun Lee, Yu-Wei Hou, Yu-Ting Fang, You-Yin Chen, Yu-Chun Lo, Didik Setyo Heriyanto, Shu-Chi Lan, Chia-Ling Chen, Xiao-Yue Chen, Kang-Yun Lee, Jer-Hwa Chang and Hsiao-Chi Chuang

Int. J. Mol. Sci. 2022, 23(16), 8906; https://doi.org/10.3390/ijms23168906 - 10 Aug 2022

Cited by 2 | Viewed by 3190

Abstract

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality in chronic lung disease patients throughout the world. Mesenchymal stem cells (MSCs) have been shown to regulate immunomodulatory, anti-inflammatory, and regenerative responses. However, the effects of human-umbilical-cord-derived mesenchymal stem cells (hUC-MSCs) on the lung pathophysiology of COPD remain unclear. We aimed to investigate the role of hUC-MSCs in emphysema severity and Yes-associated protein (Yap) phosphorylation (p-Yap) in a porcine-pancreatic-elastase (PPE)-induced emphysema model. We observed that the emphysema percentages (normalized to the total lung volume) measured by chest computed tomography (CT) and exercise oxygen desaturation were significantly reduced by hUC-MSCs at 10⁷ cells/kg body weight (BW) via intravenous administration in emphysematous mice (p < 0.05). Consistently, the emphysema index, as assessed by the mean linear intercept (MLI), significantly decreased with hUC-MSC administration at 3 × 10⁶ and 10⁷ cells/kg BW (p < 0.05). Changes in the lymphocytes, monocytes, and splenic cluster of differentiation 4-positive (CD4⁺) lymphocytes by PPE were significantly reversed by hUC-MSC administration in emphysematous mice (p < 0.05). An increasing neutrophil/lymphocyte ratio was reduced by hUC-MSCs at 3 × 10⁶ and 10⁷ cells/kg BW (p < 0.05). The higher levels of tumor necrosis factor (TNF)-α, keratinocyte chemoattractant (KC), and lactate dehydrogenase (LDH) in bronchoalveolar lavage fluid (BALF) were significantly decreased by hUC-MSC administration (p < 0.05). A decreasing p-Yap/Yap ratio in type II alveolar epithelial cells (AECII) of mice with PPE-induced emphysema was significantly increased by hUC-MSCs (p < 0.05). In conclusion, the administration of hUC-MSCs improved multiple pathophysiological features of mice with PPE-induced emphysema. The effectiveness of the treatment of pulmonary emphysema with hUC-MSCs provides an essential and significant foundation for future clinical studies of MSCs in COPD patients. Full article

(This article belongs to the Special Issue Molecular Pathophysiology of Chronic Lung Disease)

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21 pages, 3332 KiB

Open AccessArticle

Consensus Gene Co-Expression Network Analysis Identifies Novel Genes Associated with Severity of Fibrotic Lung Disease

by Sudhir Ghandikota, Mihika Sharma, Harshavardhana H. Ediga, Satish K. Madala and Anil G. Jegga

Int. J. Mol. Sci. 2022, 23(10), 5447; https://doi.org/10.3390/ijms23105447 - 13 May 2022

Cited by 14 | Viewed by 3934

Abstract

Idiopathic pulmonary fibrosis (IPF) is a severe fibrotic lung disease characterized by irreversible scarring of the lung parenchyma leading to dyspnea, progressive decline in lung function, and respiratory failure. We analyzed lung transcriptomic data from independent IPF cohorts using weighted gene co-expression network analysis (WGCNA) to identify gene modules based on their preservation status in these cohorts. The consensus gene modules were characterized by leveraging existing clinical and molecular data such as lung function, biological processes, pathways, and lung cell types. From a total of 32 consensus gene modules identified, two modules were found to be significantly correlated with the disease, lung function, and preserved in other IPF datasets. The upregulated gene module was enriched for extracellular matrix, collagen metabolic process, and BMP signaling while the downregulated module consisted of genes associated with tube morphogenesis, blood vessel development, and cell migration. Using a combination of connectivity-based and trait-based significance measures, we identified and prioritized 103 “hub” genes (including 25 secretory candidate biomarkers) by their similarity to known IPF genetic markers. Our validation studies demonstrate the dysregulated expression of CRABP2, a retinol-binding protein, in multiple lung cells of IPF, and its correlation with the decline in lung function. Full article

(This article belongs to the Special Issue Molecular Pathophysiology of Chronic Lung Disease)

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Review

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16 pages, 1340 KiB

Open AccessReview

Pulmonary Sarcoidosis: Experimental Models and Perspectives of Molecular Diagnostics Using Quantum Dots

by Natalia Linkova, Anastasiia Diatlova, Yulia Zinchenko, Anastasiia Kornilova, Petr Snetkov, Svetlana Morozkina, Dmitrii Medvedev, Alexandr Krasichkov, Victoria Polyakova and Piotr Yablonskiy

Int. J. Mol. Sci. 2023, 24(14), 11267; https://doi.org/10.3390/ijms241411267 - 10 Jul 2023

Cited by 1 | Viewed by 2308

Abstract

Sarcoidosis is a complex inflammatory multisystem disease of unknown etiology that is characterised by epithelioid cell granulomatous lesions affecting various organs, mainly the lungs. In general, sarcoidosis is asymptomatic, but some cases result in severe complications and organ failure. So far, no accurate and validated modelling for clinical and pathohistological manifestations of sarcoidosis is suggested. Moreover, knowledge about disease-specific diagnostic markers for sarcoidosis is scarce. For instance, pulmonary granulomatosis is associated with the upregulated production of proinflammatory molecules: TNF-α, IL-6, CXCL1, CCL2, CCL18, CD163, serum angiotensin-converting enzyme (sACE), lysozyme, neopterin, and serum amyloid A (SAA). Quantum dots (QDs) are widely applied for molecular diagnostics of various diseases. QDs are semiconductor nanoparticles of a few nanometres in size, made from ZnS, CdS, ZnSe, etc., with unique physical and chemical properties that are useful for the labelling and detection in biological experiments. QDs can conjugate with various antibodies or oligonucleotides, allowing for high-sensitivity detection of various targets in organs and cells. Our review describes existing experimental models for sarcoidosis (in vitro, in vivo, and in silico), their advantages and restrictions, as well as the physical properties of quantum dots and their potential applications in the molecular diagnostics of sarcoidosis. The most promising experimental models include mice with TSC2 deletion and an in silico multiscale computational model of sarcoidosis (SarcoidSim), developed using transcriptomics and flow cytometry of human sarcoid biopsies. Both models are most efficient to test different candidate drugs for sarcoidosis. Full article

(This article belongs to the Special Issue Molecular Pathophysiology of Chronic Lung Disease)

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26 pages, 2495 KiB

Open AccessReview

The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis

by Stanislav Kotlyarov

Int. J. Mol. Sci. 2023, 24(10), 8725; https://doi.org/10.3390/ijms24108725 - 13 May 2023

Cited by 19 | Viewed by 7936

Abstract

Tobacco smoking is a major cause of chronic obstructive pulmonary disease (COPD) and atherosclerotic cardiovascular disease (ASCVD). These diseases share common pathogenesis and significantly influence each other’s clinical presentation and prognosis. There is increasing evidence that the mechanisms underlying the comorbidity of COPD and ASCVD are complex and multifactorial. Smoking-induced systemic inflammation, impaired endothelial function and oxidative stress may contribute to the development and progression of both diseases. The components present in tobacco smoke can have adverse effects on various cellular functions, including macrophages and endothelial cells. Smoking may also affect the innate immune system, impair apoptosis, and promote oxidative stress in the respiratory and vascular systems. The purpose of this review is to discuss the importance of smoking in the mechanisms underlying the comorbid course of COPD and ASCVD. Full article

(This article belongs to the Special Issue Molecular Pathophysiology of Chronic Lung Disease)

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