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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 (20 October 2024) | Viewed by 20398

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Prof. Dr. Patrizia Russo

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1. Department of Human Sciences and Promotion of the Quality of Life, San Raffaele University, Via di Val Cannuta 247, 00166 Rome, Italy
2. Clinical and Molecular Epidemiology, IRCCS San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy
Interests: DNA damage; nicotine and nicotinic receptor; COVID-19; respiratory disease; toeque teno virus
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Special Issue Information

Dear Colleagues,

Respiratory diseases have a significant impact on the population, with COPD being a disabling and ultimately fatal condition. Lung cancer has a high mortality rate. Many of these conditions are linked to smoking. Interestingly, the COVID-19 mortality and severity rates are higher among smokers than they are among non-smokers.

Molecular biology technologies enable early diagnoses and improved therapies. Within the context of personalized medicine, omics approaches enable better predictions, treatments, and patient involvement. We aim to provide a comprehensive insight into state-of-the-art research activities regarding the molecular mechanisms of the pathogenesis and treatment of pulmonary diseases. We welcome all kinds of articles, including contributions about original investigations in the field, as well as reviews. The topics of interest covered include, but are not limited to, the following:

Asthma;
Bronchiectasis;
COPD and COPD rehabilitation;
COVID-19;
Cystic fibrosis;
Genomics, including DNA damage and repair;
Lung cancer and lung cancer biomarkers;
Lung microbiota;
Pneumonia;
Pulmonary fibrosis;
Pulmonology;
Respiratory diseases;
Tobacco and nicotine.

Prof. Dr. Patrizia Russo
Guest Editor

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Published Papers (4 papers)

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Research

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21 pages, 4475 KiB

Open AccessArticle

Highly Calibrated Relationship Between Bleomycin Concentrations and Facets of the Active Phase Fibrosis in Classical Mouse Bleomycin Model

by Anil Hari Kadam and Jan E. Schnitzer

Int. J. Mol. Sci. 2024, 25(22), 12300; https://doi.org/10.3390/ijms252212300 - 15 Nov 2024

Viewed by 1961

Abstract

The mouse bleomycin model is useful in pre-clinical IPF research to understand pathophysiological mechanisms and pharmacological interventions. In the present study, we systematically investigated the effects of bleomycin at a 60-fold dose range on experimental features of lung fibrosis in the mouse bleomycin model. We analyzed the effect of intratracheal (i.t.) dosing of 0.05–3 U/kg bleomycin on disease phenotypes, including weight loss, morbidity and mortality, pulmonary inflammation, lung collagen content, various BALF biomarkers, and histology in a 14-day mouse model when the animals are in the active phase of fibrosis. In mice, challenge with 1–2 U/kg bleomycin doses induced significant and saturated responses on fibrotic endpoints, confirmed by collagen content, BALF biomarker levels, and marked weight loss compared to the normal control (NC). We observed 100% mortality in 3 U/kg of bleomycin-treated mice. In contrast, 0.05–0.5 U/kg bleomycin doses induced a dose-dependent fibrotic phenotype. The mice challenged with doses of 0.25–0.5 U/kg bleomycin showed optimum body weight loss, a significant increase in pulmonary inflammation, and the fibrotic phenotype compared to NC. Furthermore, we showed 0.25–0.5 U/kg bleomycin increases expression levels of (pro-) fibrotic cytokines, which are the mediators involved in the activation of myofibroblast during fibrogenesis (TGF-β1, IL-13, IL-6, WISP-1, VEGF), angiogenesis (VEGF), matrix remodeling (TIMP-1), and non-invasive lung function biomarker (CRP) compared to NC. A modified Ashcroft scale quantified that the fibrotic changes in the lungs were significantly higher in the lung of mice dosed at 0.25–0.5 U/kg > 0.1 U/kg bleomycin and non-significant in mice lung dosed at 0.05 U/kg bleomycin compared to NC. We demonstrated that the changes due to 0.25–0.5 U/kg i.t. bleomycin on protein biomarkers are enough to drive robust and detectable fibrotic pathology without mortality. The 0.1 U/kg has a moderate phenotype, and 0.05 U/kg had no detectable phenotype. The Goodness of Fit (r²) and Pearson correlation coefficient (r) analyses revealed a positive linear association between change evaluated in all experimental features of fibrosis and bleomycin concentrations (0.05–0.5 U/kg). Here, we provide an examination of a highly calibrated relationship between 60-fold bleomycin concentrations and a set of in vivo readouts that covers various facets of experimental fibrosis. Our study shows that there is a dose-dependent effect of bleomycin on the features of experimental fibrosis at <1 U/kg, whereas saturated responses are achieved at >1 U/kg. Our careful experimental observations, accuracy, and comprehensive data set provided meaningful insights into the effect of bleomycin dose(s) on the fibrotic phenotype, which is valuable in preclinical drug development and lung fibrosis research. In addition, we have presented a set of reproducible frameworks of endpoints that can be used for reliable assessment of the fibrotic phenotype, and in vivo therapeutic intervention(s) with improved accuracy. Full article

(This article belongs to the Special Issue State-of-the-Art Molecular Mechanisms of Pulmonary Pathology)

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14 pages, 2910 KiB

Open AccessArticle

Levels of Lysozyme and SLPI in Bronchoalveolar Lavage: Exploring Their Role in Interstitial Lung Disease

by Rubén Osuna-Gómez, Maria Mulet, Silvia Barril, Elisabet Cantó, Paloma Millan-Billi, Ana Pardessus, David de la Rosa-Carrillo, Diego Castillo and Silvia Vidal

Int. J. Mol. Sci. 2024, 25(8), 4297; https://doi.org/10.3390/ijms25084297 - 12 Apr 2024

Cited by 1 | Viewed by 1860

Abstract

Interstitial lung diseases (ILDs) are characterized by inflammation or fibrosis of the pulmonary parenchyma. Despite the involvement of immune cells and soluble mediators in pulmonary fibrosis, the influence of antimicrobial peptides (AMPs) remains underexplored. These effector molecules display a range of activities, which include immunomodulation and wound repair. Here, we investigate the role of AMPs in the development of fibrosis in ILD. We compare the concentration of different AMPs and different cytokines in 46 fibrotic (F-ILD) and 17 non-fibrotic (NF-ILD) patients by ELISA and using peripheral blood mononuclear cells from in vitro stimulation in the presence of lysozyme or secretory leukocyte protease inhibitor (SLPI) from 10 healthy donors. We observed that bronchoalveolar lavage (BAL) levels of AMPs were decreased in F-ILD patients (lysozyme: p < 0.001; SLPI: p < 0.001; LL-37: p < 0.001; lactoferrin: p = 0.47) and were negatively correlated with levels of TGF-β (lysozyme: p = 0.02; SLPI: p < 0.001) and IL-17 (lysozyme: p < 0.001; SLPI: p < 0.001). We observed that lysozyme increased the percentage of CD86⁺ macrophages (p < 0.001) and the production of TNF-α (p < 0.001). We showed that lysozyme and SLPI were associated with clinical parameters (lysozyme: p < 0.001; SLPI: p < 0.001) and disease progression (lysozyme: p < 0.001; SLPI: p = 0.01). These results suggest that AMPs may play an important role in the anti-fibrotic response, regulating the effect of pro-fibrotic cytokines. In addition, levels of lysozyme in BAL may be a potential biomarker to predict the progression in F-ILD patients. Full article

(This article belongs to the Special Issue State-of-the-Art Molecular Mechanisms of Pulmonary Pathology)

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Review

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16 pages, 1413 KiB

Open AccessReview

ADAM33′s Role in Asthma Pathogenesis: An Overview

by Jakub Sleziak, Antoni Gawor, Marta Błażejewska, Katarzyna Antosz and Krzysztof Gomułka

Int. J. Mol. Sci. 2024, 25(4), 2318; https://doi.org/10.3390/ijms25042318 - 15 Feb 2024

Cited by 3 | Viewed by 2824

Abstract

Asthma is a complex chronic respiratory disease characterized by airway hyperresponsiveness, inflammation, and obstruction. Many genes have been identified as associated with asthma but none with such substantial significance as the ADAM33 gene due to its role in airway remodeling and bronchial hyperresponsiveness. This review summarizes the current knowledge on the genetic and functional aspects of ADAM33 in asthma pathogenesis. We highlight its genetic variants associated with asthma susceptibility and severity, as well as the functional effects of ADAM33 on airway remodeling, smooth muscle cell proliferation, and its interplay with environmental factors. Additionally, we discuss the potential clinical implications of ADAM33 as a therapeutic target for asthma management. Full article

(This article belongs to the Special Issue State-of-the-Art Molecular Mechanisms of Pulmonary Pathology)

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20 pages, 1163 KiB

Open AccessReview

Nicotine: From Discovery to Biological Effects

by Luigi Sansone, Francesca Milani, Riccardo Fabrizi, Manuel Belli, Mario Cristina, Vincenzo Zagà, Antonio de Iure, Luca Cicconi, Stefano Bonassi and Patrizia Russo

Int. J. Mol. Sci. 2023, 24(19), 14570; https://doi.org/10.3390/ijms241914570 - 26 Sep 2023

Cited by 20 | Viewed by 12900

Abstract

Nicotine, the primary psychoactive agent in tobacco leaves, has led to the widespread use of tobacco, with over one billion smokers globally. This article provides a historical overview of tobacco and discusses tobacco dependence, as well as the biological effects induced by nicotine on mammalian cells. Nicotine induces various biological effects, such as neoangiogenesis, cell division, and proliferation, and it affects neural and non-neural cells through specific pathways downstream of nicotinic receptors (nAChRs). Specific effects mediated by α7 nAChRs are highlighted. Nicotine is highly addictive and hazardous. Public health initiatives should prioritize combating smoking and its associated risks. Understanding nicotine’s complex biological effects is essential for comprehensive research and informed health policies. While potential links between nicotine and COVID-19 severity warrant further investigation, smoking remains a significant cause of morbidity and mortality globally. Effective public health strategies are vital to promote healthier lifestyles. Full article

(This article belongs to the Special Issue State-of-the-Art Molecular Mechanisms of Pulmonary Pathology)

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