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Molecular Research on Lung, Microbiome and Pulmonary Diseases
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Molecular Research on Lung, Microbiome and Pulmonary Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 11679

Special Issue Editor

Dr. Patrizia Russo

E-Mail Website
Guest Editor
1. IRCCS "San Raffaele Pisana", Via di Valcannuta 247, I-00166 Roma, Italy
2. Department of Human Sciences and Quality of Life Promotion San Raffaele University, Via di Val Cannuta, 247, I-00166 Rome, Italy
Interests: research in nicotinic receptor in cancer; COPD; addiction; Alzheimer; systems medicine; Covid-19
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diseases of the respiratory system are among some of the most common medical conditions in the world. Tens of millions of people have lung disease in the U.S. alone. Moreover, diseases of the respiratory system accounted for 7.5 % of all deaths in the EU-27 in 2016. Smoking, infections, and genes cause most lung diseases. Pulmonary pathology includes a large spectrum of both neoplastic and non-neoplastic diseases (i.e., COPD) that affect the lung. Pulmonary pathology studies the changes in the lung tissues and the mechanisms through which these occur. Although, initially, the lung was considered sterile, actually, the existence of a healthy lung microbiome is usually accepted, and changes are reported in COPD and in its exacerbation. The lung is the main affected organ in severe coronavirus disease 2019 (COVID-19) caused by the novel coronavirus SARS-CoV-2, and lung damage is the leading cause of death in the vast majority of patients. Post-mortem examinations of COVID-19 patients revealed diffuse alveolar damage with severe capillary congestion, microthrombosis, and thrombosis of small to mid-sized arteries as well as pulmonary thromboembolism, suggesting vascular dysfunction.

In this Special Issue, we invite contributors to publish their research on microbe-related lung diseases molecular biology, the molecular basis of pathogenicity, latent infection, immune evasion strategies, and the development of new vaccines.

Dr. Patrizia Russo
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. 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

  • COPD
  • cellular mechanism
  • genetics
  • lung cancer
  • lung microbiota
  • molecular mechanisms
  • smoking

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Published Papers (3 papers)

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Research

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14 pages, 2286 KiB  
Article
Nicotine in Combination with SARS-CoV-2 Affects Cells Viability, Inflammatory Response and Ultrastructural Integrity
by Luigi Sansone, Antonio de Iure, Mario Cristina, Manuel Belli, Laura Vitiello, Federica Marcolongo, Alfredo Rosellini, Lisa Macera, Pietro Giorgio Spezia, Carlo Tomino, Stefano Bonassi, Matteo A. Russo, Fabrizio Maggi and Patrizia Russo
Int. J. Mol. Sci. 2022, 23(16), 9488; https://doi.org/10.3390/ijms23169488 - 22 Aug 2022
Cited by 4 | Viewed by 2438
Abstract
The aims of our study are to: (i) investigate the ability of nicotine to modulate the expression level of inflammatory cytokines in A549 cells infected with SARS-CoV-2; (ii) elucidate the ultrastructural features caused by the combination nicotine+SARS-CoV-2; and (iii) demonstrate the mechanism of [...] Read more.
The aims of our study are to: (i) investigate the ability of nicotine to modulate the expression level of inflammatory cytokines in A549 cells infected with SARS-CoV-2; (ii) elucidate the ultrastructural features caused by the combination nicotine+SARS-CoV-2; and (iii) demonstrate the mechanism of action. In this study, A549 cells pretreated with nicotine were either exposed to LPS or poly(I:C), or infected with SARS-CoV-2. Treated and untreated cells were analyzed for cytokine production, cytotoxicity, and ultrastructural modifications. Vero E6 cells were used as a positive reference. Cells pretreated with nicotine showed a decrease of IL6 and TNFα in A549 cells induced by LPS or poly(I:C). In contrast, cells exposed to SARS-CoV-2 showed a high increase of IL6, IL8, IL10 and TNFα, high cytopathic effects that were dose- and time-dependent, and profound ultrastructural modifications. These modifications were characterized by membrane ruptures and fragmentation, the swelling of cytosol and mitochondria, the release of cytoplasmic content in extracellular spaces (including osmiophilic granules), the fragmentation of endoplasmic reticulum, and chromatin disorganization. Nicotine increased SARS-CoV-2 cytopathic effects, elevating the levels of inflammatory cytokines, and inducing severe cellular damage, with features resembling pyroptosis and necroptosis. The protective role of nicotine in COVID-19 is definitively ruled out. Full article
(This article belongs to the Special Issue Molecular Research on Lung, Microbiome and Pulmonary Diseases)
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20 pages, 4230 KiB  
Article
Genomic and Immunological Characterization of Hypermucoviscous Carbapenem-Resistant Klebsiella pneumoniae ST25 Isolates from Northwest Argentina
by Leonardo Albarracin, Ramiro Ortiz Moyano, Juan Martin Vargas, Bruno G. N. Andrade, Juan Cortez Zamar, Stefania Dentice Maidana, Kohtaro Fukuyama, Shoichiro Kurata, María Ángela Jure, Haruki Kitazawa and Julio Villena
Int. J. Mol. Sci. 2022, 23(13), 7361; https://doi.org/10.3390/ijms23137361 - 1 Jul 2022
Cited by 8 | Viewed by 2868
Abstract
In recent years, an increase in the prevalence hypermucoviscous carbapenem-resistant Klebsiella pneumoniae with sequence type 25 (ST25) was detected in hospitals of Tucuman (Northwest Argentina). In this work, the virulence and the innate immune response to two K. pneumoniae ST25 strains (LABACER 01 [...] Read more.
In recent years, an increase in the prevalence hypermucoviscous carbapenem-resistant Klebsiella pneumoniae with sequence type 25 (ST25) was detected in hospitals of Tucuman (Northwest Argentina). In this work, the virulence and the innate immune response to two K. pneumoniae ST25 strains (LABACER 01 and LABACER 27) were evaluated in a murine model after a respiratory challenge. In addition, comparative genomics was performed with K. pneumoniae LABACER01 and LABACER27 to analyze genes associated with virulence. Both LABACER01 and LABACER27 were detected in the lungs of infected mice two days after the nasal challenge, with LABACER01 counts significantly higher than those of LABACER27. Only LABACER01 was detected in hemocultures. Lactate dehydrogenase (LDH) and albumin levels in bronchoalveolar lavage (BAL) samples were significantly higher in mice challenged with LABACER01 than in LABACER27-infected animals, indicating greater lung tissue damage. Both strains increased the levels of neutrophils, macrophages, TNF-α, IL-1β, IL-6, KC, MCP-1, IFN-γ, and IL-17 in the respiratory tract and blood, with the effect of LABACER01 more marked than that of LABACER27. In contrast, LABACER27 induced higher levels of IL-10 in the respiratory tract than LABACER01. Genomic analysis revealed that K. pneumoniae LABACER01 and LABACER27 possess virulence factors found in other strains that have been shown to be hypervirulent, including genes required for enterobactin (entABCDEF) and salmochelin (iroDE) biosynthesis. In both strains, the genes of toxin–antitoxin systems, as well as regulators of the expression of virulence factors and adhesion genes were also detected. Studies on the genetic potential of multiresistant K. pneumoniae strains as well as their cellular and molecular interactions with the host are of fundamental importance to assess the association of certain virulence factors with the intensity of the inflammatory response. In this sense, this work explored the virulence profile based on genomic and in vivo studies of hypermucoviscous carbapenem-resistant K. pneumoniae ST25 strains, expanding the knowledge of the biology of the emerging ST25 clone in Argentina. Full article
(This article belongs to the Special Issue Molecular Research on Lung, Microbiome and Pulmonary Diseases)
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Review

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18 pages, 1704 KiB  
Review
The Role of CD4+ T Cells and Microbiota in the Pathogenesis of Asthma
by Jiung Jeong and Heung Kyu Lee
Int. J. Mol. Sci. 2021, 22(21), 11822; https://doi.org/10.3390/ijms222111822 - 31 Oct 2021
Cited by 29 | Viewed by 5547
Abstract
Asthma, a chronic respiratory disease involving variable airflow limitations, exhibits two phenotypes: eosinophilic and neutrophilic. The asthma phenotype must be considered because the prognosis and drug responsiveness of eosinophilic and neutrophilic asthma differ. CD4+ T cells are the main determinant of asthma [...] Read more.
Asthma, a chronic respiratory disease involving variable airflow limitations, exhibits two phenotypes: eosinophilic and neutrophilic. The asthma phenotype must be considered because the prognosis and drug responsiveness of eosinophilic and neutrophilic asthma differ. CD4+ T cells are the main determinant of asthma phenotype. Th2, Th9 and Tfh cells mediate the development of eosinophilic asthma, whereas Th1 and Th17 cells mediate the development of neutrophilic asthma. Elucidating the biological roles of CD4+ T cells is thus essential for developing effective asthma treatments and predicting a patient’s prognosis. Commensal bacteria also play a key role in the pathogenesis of asthma. Beneficial bacteria within the host act to suppress asthma, whereas harmful bacteria exacerbate asthma. Recent literature indicates that imbalances between beneficial and harmful bacteria affect the differentiation of CD4+ T cells, leading to the development of asthma. Correcting bacterial imbalances using probiotics reportedly improves asthma symptoms. In this review, we investigate the effects of crosstalk between the microbiota and CD4+ T cells on the development of asthma. Full article
(This article belongs to the Special Issue Molecular Research on Lung, Microbiome and Pulmonary Diseases)
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