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Special Issue "Chronic Inflammatory Lung Diseases: Molecular Pathology"

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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
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Dr. Lei Fang

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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

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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

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Research

Open AccessArticle

Lung Epithelial Cells from Obese Patients Have Impaired Control of SARS-CoV-2 Infection

and

Int. J. Mol. Sci. 2023, 24(7), 6729; https://doi.org/10.3390/ijms24076729 - 04 Apr 2023

Cited by 1 | Viewed by 1101

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 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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Open AccessArticle

An Amide Alkaloid Isolated from Ephedra sinica Ameliorates OVA-Induced Allergic Asthma by Inhibiting Mast Cell Activation and Dendritic Cell Maturation

and

Int. J. Mol. Sci. 2022, 23(21), 13541; https://doi.org/10.3390/ijms232113541 - 04 Nov 2022

Cited by 3 | Viewed by 1137

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 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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Special Issue "Chronic Inflammatory Lung Diseases: Molecular Pathology"

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