Molecular and Cellular Mechanisms of Chronic Obstructive Pulmonary Disease (COPD)

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 25 July 2024 | Viewed by 2311

Special Issue Editor


E-Mail Website
Guest Editor
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
Interests: chronic lung disease; COPD; house hold air pollution (HAP); LIC; LMIC; electronic cigarettes; heated tobacco products
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. Tobacco smoking, exposure to biomass smoke, air pollution, and occupation exposures are regarded as some of the major causes of COPD. Chronic bronchitis and emphysema are commonly associated with COPD. Classical inflammatory reactions and oxidative stress are considered as the major molecular pathways upstream of COPD pathogenesis. However, current knowledge points towards the involvement of much broader mechanisms. In order to discover new targets, identify robust biomarkers, and develop novel therapies, there is a need to develop a deeper understanding of the molecular and cellular mechanisms.

This Special Issue aims to summarize the current knowledge and advances in the COPD area of research, including studies that cover diagnostic tools, basic molecular mechanisms, pharmacotherapy, toxicological risk assessments, genomics, and computational modeling of diseased lung. We invite you to submit original research articles and comprehensive review articles that cover the newest findings in these fields.

Dr. Koustav Ganguly
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • chronic obstructive pulmonary disease
  • COPD
  • smoke
  • pharmacotherapy
  • toxicological
  • genomics
  • computational modeling

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

12 pages, 1876 KiB  
Article
Single-Cell Sequencing of Lung Macrophages and Monocytes Reveals Novel Therapeutic Targets in COPD
by Yushan Hu, Xiaojian Shao, Li Xing, Xuan Li, Geoffrey M. Nonis, Graeme J. Koelwyn, Xuekui Zhang and Don D. Sin
Cells 2023, 12(24), 2771; https://doi.org/10.3390/cells12242771 - 5 Dec 2023
Cited by 3 | Viewed by 1793
Abstract
Background: Macrophages and monocytes orchestrate inflammatory processes in the lungs. However, their role in the pathogenesis of chronic obstructive pulmonary disease (COPD), an inflammatory condition, is not well known. Here, we determined the characteristics of these cells in lungs of COPD patients and [...] Read more.
Background: Macrophages and monocytes orchestrate inflammatory processes in the lungs. However, their role in the pathogenesis of chronic obstructive pulmonary disease (COPD), an inflammatory condition, is not well known. Here, we determined the characteristics of these cells in lungs of COPD patients and identified novel therapeutic targets. Methods: We analyzed the RNA sequencing (scRNA-seq) data of explanted human lung tissue from COPD (n = 18) and control (n = 28) lungs and found 16 transcriptionally distinct groups of macrophages and monocytes. We performed pathway and gene enrichment analyses to determine the characteristics of macrophages and monocytes from COPD (versus control) lungs and to identify the therapeutic targets, which were then validated using data from a randomized controlled trial of COPD patients (DISARM). Results: In the alveolar macrophages, 176 genes were differentially expressed (83 up- and 93 downregulated; Padj < 0.05, |log2FC| > 0.5) and were enriched in downstream biological processes predicted to cause poor lipid uptake and impaired cell activation, movement, and angiogenesis in COPD versus control lungs. Classical monocytes from COPD lungs harbored a differential gene set predicted to cause the activation, mobilization, and recruitment of cells and a hyperinflammatory response to influenza. In silico, the corticosteroid fluticasone propionate was one of the top compounds predicted to modulate the abnormal transcriptional profiles of these cells. In vivo, a fluticasone–salmeterol combination significantly modulated the gene expression profiles of bronchoalveolar lavage cells of COPD patients (p < 0.05). Conclusions: COPD lungs harbor transcriptionally distinct lung macrophages and monocytes, reflective of a dysfunctional and hyperinflammatory state. Inhaled corticosteroids and other compounds can modulate the transcriptomic profile of these cells in patients with COPD. Full article
Show Figures

Figure 1

Back to TopTop