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Chronic Inflammatory Lung Diseases: Molecular Pathology
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Chronic Inflammatory Lung Diseases: Molecular Pathology

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 October 2023) | Viewed by 6467

Special Issue Editors

Prof. Dr. Michael Roth

E-Mail Website
Guest Editor
Pulmonary Cell Research/Pneumology, Department of Biomedicine/Internal Medicine, University & University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland
Interests: tissue remodeling in chronic lung diseases; asthma; COPD; lung fibrosis; epi-genetics; cell signaling; cell differentiation; epithelial cells; fibroblasts; airway smooth muscle cells
Special Issues, Collections and Topics in MDPI journals
Dr. Lei Fang

E-Mail Website
Guest Editor
Pulmonary Cell Research/Pneumology, Department of Biomedicine/Internal Medicine, University & University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland
Interests: airway remodeling; smooth muscle cells; asthma

Special Issue Information

Dear Colleagues,

Chronic inflammatory lung diseases, including asthma, COPD, and fibrosis, are the most frequent non-communicable chronic diseases. None of them can be cured due to a lack of understanding around molecular pathogenesis. Inflammation alone is insufficient to explain the development and the often life-long burden. Fibrotic processes or excessive tissue remodeling are well-noted pathologies in all of these diseases, but their origins cannot be explained by inflammation. New ideas are needed to understand and resolve these pathologies.

In this Special Issue, we would like you to think unconventionally and contribute your innovative ideas regarding the origin of the disease and the reasons why they could not be cured with available strategies. However, we would like to remind you that the focus of this journal is molecular science; therefore, we will not accept purely clinical studies without a strong link to molecular sciences. 

Prof. Dr. Michael Roth
Dr. Lei Fang
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
  • COPD
  • lung fibrosis
  • tissue remodeling
  • tissue degradation
  • cell-cell interaction
  • chronic inflammation lung diseases
  • cellular signaling
  • cell differentiation
  • cell aging
  • cell metabolism
  • mitochondrial action
  • cellular sugars
  • extracellular matrix

Published Papers (3 papers)

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Research

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14 pages, 3999 KiB  
Article
Lung Epithelial Cells from Obese Patients Have Impaired Control of SARS-CoV-2 Infection
by Mellissa Gaudet, Eva Kaufmann, Nour Jalaleddine, Andrea Mogas, Mahmood Hachim, Abiola Senok, Maziar Divangahi, Qutayba Hamid and Saba Al Heialy
Int. J. Mol. Sci. 2023, 24(7), 6729; https://doi.org/10.3390/ijms24076729 - 04 Apr 2023
Cited by 1 | Viewed by 1644
Abstract
Obesity is known to increase the complications of the COVID-19 coronavirus disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the exact mechanisms of SARS-CoV-2 infection in obese patients have not been clearly elucidated. This study aims to better understand the [...] Read more.
Obesity is known to increase the complications of the COVID-19 coronavirus disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the exact mechanisms of SARS-CoV-2 infection in obese patients have not been clearly elucidated. This study aims to better understand the effect of obesity on the course of SARS-CoV-2 infection and identify candidate molecular pathways involved in the progression of the disease, using an in vitro live infection model and RNA sequencing. Results from this study revealed the enhancement of viral load and replication in bronchial epithelial cells (NHBE) from obese subjects at 24 h of infection (MOI = 0.5) as compared to non-obese subjects. Transcriptomic profiling via RNA-Seq highlighted the enrichment of lipid metabolism-related pathways along with LPIN2, an inflammasome regulator, as a unique differentially expressed gene (DEG) in infected bronchial epithelial cells from obese subjects. Such findings correlated with altered cytokine and angiotensin-converting enzyme-2 (ACE2) expression during infection of bronchial cells. These findings provide a novel insight on the molecular interplay between obesity and SARS-CoV-2 infection. In conclusion, this study demonstrates the increased SARS-CoV-2 infection of bronchial epithelial cells from obese subjects and highlights the impaired immunity which may explain the increased severity among obese COVID-19 patients. Full article
(This article belongs to the Special Issue Chronic Inflammatory Lung Diseases: Molecular Pathology)
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16 pages, 6285 KiB  
Article
An Amide Alkaloid Isolated from Ephedra sinica Ameliorates OVA-Induced Allergic Asthma by Inhibiting Mast Cell Activation and Dendritic Cell Maturation
by Jufang Jia, Mengnan Zeng, Denghui Zhu, Xinmian Jiao, Beibei Zhang, Ruolan Yang, Weisheng Feng and Xiaoke Zheng
Int. J. Mol. Sci. 2022, 23(21), 13541; https://doi.org/10.3390/ijms232113541 - 04 Nov 2022
Cited by 8 | Viewed by 1655
Abstract
Asthma, which is a chronic inflammatory disease of the airways, is usually caused by allergens in which various structures and immune cells are involved. Ephedra sinica, the most commonly used Chinese medicine, has significant clinical effects on asthma, but its components are [...] Read more.
Asthma, which is a chronic inflammatory disease of the airways, is usually caused by allergens in which various structures and immune cells are involved. Ephedra sinica, the most commonly used Chinese medicine, has significant clinical effects on asthma, but its components are complex and the mechanism of action has not been fully elucidated. Among its components, we identified an amide alkaloid (EB-A) and investigated its anti-asthmatic activity and the underlying mechanisms. In this study, we replicated an OVA-sensitized/challenged allergic asthma mouse model, and divided the mice into a model (OVA) group, positive drug (Y, 0.5 mg/kg/day) group, and EB-A treatment with low (Low, 10 mg/kg/day) and high dose (High, 20 mg/kg/day) groups. Asthma-related features were analyzed through the airway hyperresponsiveness (AHR), cough and wheeze indexes, allergen-specific IgE, prostaglandin D2 (PDG2), and lung histology in mice. The levels of apoptosis and reactive oxygen species (ROS) in the primary lung cells, cytokines in the serum and broncho-alveolar lavage fluid (BALF), and proteinase-activated receptor-2 (PAR2) pathway activation in the lung tissue were measured to evaluate the inflammatory injury and lung epithelial barrier damage in the mice. Dendritic cell (DC) maturation and mast cell (MC) activation were verified in vitro and in vivo. Furthermore, the effect of a PAR2 activation in lung epithelial cells on the maturation of DCs was evaluated by the co-culture system of (human bronchial epithelial cell lines) 16HBE and bone marrow-derived dendritic cells (BMDCs). The results showed that EB-A inhibited the typical asthmatic phenotypes, as well as lung injury and inflammation, MC activation and degranulation, and DC maturation in the OVA-sensitized/challenged BALB/c mice. In addition, EB-A inhibited the expression of PAR2 in the lung epithelial cells and significantly interfered with the maturation of DCs after inhibiting PAR2. Taken together, our study firstly demonstrated that EB-A could ameliorate OVA-induced allergic asthma by inhibiting MC activation and DC maturation, and the molecular mechanism of EB-A’s anti-asthmatic activity might be mediated by inhibiting PAR2. Our data provide a molecular justification for the use of EB-A in the treatment of allergic asthma. Full article
(This article belongs to the Special Issue Chronic Inflammatory Lung Diseases: Molecular Pathology)
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Review

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21 pages, 756 KiB  
Review
Bronchial Asthma, Airway Remodeling and Lung Fibrosis as Successive Steps of One Process
by Innokenty A. Savin, Marina A. Zenkova and Aleksandra V. Sen’kova
Int. J. Mol. Sci. 2023, 24(22), 16042; https://doi.org/10.3390/ijms242216042 - 07 Nov 2023
Cited by 1 | Viewed by 2522
Abstract
Bronchial asthma is a heterogeneous disease characterized by persistent respiratory system inflammation, airway hyperreactivity, and airflow obstruction. Airway remodeling, defined as changes in airway wall structure such as extensive epithelial damage, airway smooth muscle hypertrophy, collagen deposition, and subepithelial fibrosis, is a key [...] Read more.
Bronchial asthma is a heterogeneous disease characterized by persistent respiratory system inflammation, airway hyperreactivity, and airflow obstruction. Airway remodeling, defined as changes in airway wall structure such as extensive epithelial damage, airway smooth muscle hypertrophy, collagen deposition, and subepithelial fibrosis, is a key feature of asthma. Lung fibrosis is a common occurrence in the pathogenesis of fatal and long-term asthma, and it is associated with disease severity and resistance to therapy. It can thus be regarded as an irreversible consequence of asthma-induced airway inflammation and remodeling. Asthma heterogeneity presents several diagnostic challenges, particularly in distinguishing between chronic asthma and other pulmonary diseases characterized by disruption of normal lung architecture and functions, such as chronic obstructive pulmonary disease. The search for instruments that can predict the development of irreversible structural changes in the lungs, such as chronic components of airway remodeling and fibrosis, is particularly difficult. To overcome these challenges, significant efforts are being directed toward the discovery and investigation of molecular characteristics and biomarkers capable of distinguishing between different types of asthma as well as between asthma and other pulmonary disorders with similar structural characteristics. The main features of bronchial asthma etiology, pathogenesis, and morphological characteristics as well as asthma-associated airway remodeling and lung fibrosis as successive stages of one process will be discussed in this review. The most common murine models and biomarkers of asthma progression and post-asthmatic fibrosis will also be covered. The molecular mechanisms and key cellular players of the asthmatic process described and systematized in this review are intended to help in the search for new molecular markers and promising therapeutic targets for asthma prediction and therapy. Full article
(This article belongs to the Special Issue Chronic Inflammatory Lung Diseases: Molecular Pathology)
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