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Molecular Mechanisms in Chronic Obstructive Pulmonary Disease

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 (31 March 2024) | Viewed by 789

Special Issue Editor

Special Issue Information

Dear Colleagues,

Chronic obstructive pulmonary disease (COPD) represents a significant global public health concern, resulting in substantial morbidity and mortality. COPD is believed to be the outcome of complex interactions between genetic and environmental (GxE) factors that unfold over a person's entire lifetime, from conception to death. Notably, the impacts of active smoking and exposure to secondhand smoke are well established within this context. These interactions extend beyond the respiratory system, affecting various organ systems and leading to the simultaneous development of multiple coexisting diseases as individuals age. Moreover, specific diseases tend to co-occur in COPD patients due to shared risk factors and biological interactions, compounding the disease's prognosis and societal burden, creating what is referred to as a "syndemic."

Certain chronic respiratory conditions, such as COPD, have been associated with persistent infections caused by human respiratory syncytial virus, SARS-CoV-2 and human rhinovirus. However, it remains uncertain whether RNA viruses establish long-term infections, as is acknowledged for DNA viruses like human bocavirus and adenoviruses. Torquetenovirus (TTV), a DNA virus, is implicated in immunosenescence and may play a role in the severity of COPD.

The substantial diversity within COPD has posed challenges in developing pharmaceutical treatments capable of effectively slowing the progression of the disease. Within this context, rehabilitation plays a prominent role. Precision medicine strategies offer a potential solution by focusing on understanding an individual's risk factors for the disease and tailoring treatment plans based on factors such as disease mechanisms, environmental exposures, and psychological variables. It is of paramount importance to promptly identify COPD patients at high risk of adverse outcomes and to gain a comprehensive understanding, at a mechanistic level, as to why specific individuals present an elevated risk.

Dr. Patrizia Russo
Guest Editor

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Keywords

  • COPD epidemiology
  • COPD causes
  • COPD diagnosis
  • biomarkers for prediction, diagnosis and response
  • pharmacology
  • rehabilitation
  • virus

Published Papers (1 paper)

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Research

17 pages, 3050 KiB  
Article
Gut Microbiome and Transcriptomic Changes in Cigarette Smoke-Exposed Mice Compared to COPD and CD Patient Datasets
by Lei Wang, Pim J. Koelink, Johan Garssen, Gert Folkerts, Paul A. J. Henricks and Saskia Braber
Int. J. Mol. Sci. 2024, 25(7), 4058; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25074058 - 05 Apr 2024
Viewed by 635
Abstract
Chronic obstructive pulmonary disease (COPD) patients and smokers have a higher incidence of intestinal disorders. The aim of this study was to gain insight into the transcriptomic changes in the lungs and intestines, and the fecal microbial composition after cigarette smoke exposure. Mice [...] Read more.
Chronic obstructive pulmonary disease (COPD) patients and smokers have a higher incidence of intestinal disorders. The aim of this study was to gain insight into the transcriptomic changes in the lungs and intestines, and the fecal microbial composition after cigarette smoke exposure. Mice were exposed to cigarette smoke and their lung and ileum tissues were analyzed by RNA sequencing. The top 15 differentially expressed genes were investigated in publicly available gene expression datasets of COPD and Crohn’s disease (CD) patients. The murine microbiota composition was determined by 16S rRNA sequencing. Increased expression of MMP12, GPNMB, CTSK, CD68, SPP1, CCL22, and ITGAX was found in the lungs of cigarette smoke-exposed mice and COPD patients. Changes in the intestinal expression of CD79B, PAX5, and FCRLA were observed in the ileum of cigarette smoke-exposed mice and CD patients. Furthermore, inflammatory cytokine profiles and adhesion molecules in both the lungs and intestines of cigarette smoke-exposed mice were profoundly changed. An altered intestinal microbiota composition and a reduction in bacterial diversity was observed in cigarette smoke-exposed mice. Altered gene expression in the murine lung was detected after cigarette smoke exposure, which might simulate COPD-like alterations. The transcriptomic changes in the intestine of cigarette smoke-exposed mice had some similarities with those of CD patients and were associated with changes in the intestinal microbiome. Future research could benefit from investigating the specific mechanisms underlying the observed gene expression changes due to cigarette smoke exposure, focusing on identifying potential therapeutic targets for COPD and CD. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Chronic Obstructive Pulmonary Disease)
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