Pneumonia Basic Science

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 13228

Special Issue Editors

Department of Pathophysiology and Transplantation, Università degli Studi di Milano, IRCCS Fondazione Ospedale Maggiore Policlinico Cà Granda, 20122 Milan, Italy
Interests: pneumonia; COPD; bronchiectasis; cystic fibrosis; lung transplantation
Special Issues, Collections and Topics in MDPI journals
Director Pulmonary Intensive Care Unit, Respiratory Institute, Hospital Clinic of Barcelona, Barcelona, Spain
Interests: respiratory medicine; epidemiology; risk factors; outcome; treatment; prevention and pathogenetic mechanisms of respiratory infections; community-acquired pneumonia; intensive care
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pneumonia is a clinical and public health issue worldwide, affecting approximately 400 million people and causing more than 2 million deaths/year. Studies on pathophysiology are providing new insights into the mechanisms underlying the host response and have led to the discovery of new molecules designed to face infection and inflammation related to pneumonia. This Special Issue of Biomedicines focuses on recent advances in the role of microbiome, host genetics, immune response, new biomarkers, and new treatment of this disease.

The goal is to stimulate research and clinical interests in this exciting field with the hope of developing strategies for prevention, better understanding the pathophysiological mechanisms and improving treatment outcomes both in immunocompetent and immunocompromised patients with pneumonia.

You may choose our Joint Special Issue in Medical Sciences.

Prof. Dr. Francesco Blasi
Prof. Dr. Antoni Torres
Guest Editors

Manuscript Submission Information

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Keywords

  • pneumonia
  • microbiome
  • genetics
  • immunopathology

Published Papers (4 papers)

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Research

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10 pages, 591 KiB  
Article
Role of VEGF Polymorphisms in the Susceptibility and Severity of Interstitial Lung Disease
Biomedicines 2021, 9(5), 458; https://doi.org/10.3390/biomedicines9050458 - 22 Apr 2021
Cited by 5 | Viewed by 1972
Abstract
The search for biomarkers that can help to establish an early diagnosis and prognosis of interstitial lung disease (ILD) is of potential interest. VEGF polymorphisms have been implicated in the development of several lung disorders. Consequently, we assessed, for the first time, the [...] Read more.
The search for biomarkers that can help to establish an early diagnosis and prognosis of interstitial lung disease (ILD) is of potential interest. VEGF polymorphisms have been implicated in the development of several lung disorders. Consequently, we assessed, for the first time, the role of VEGF polymorphisms in the susceptibility and severity of ILD. A total of 436 Caucasian ILD patients (244 with idiopathic interstitial pneumonias (IIPs) and 192 with non-IIP) and 536 ethnically-matched healthy controls were genotyped for VEGF rs833061, rs1570360, rs2010963, rs3025020, and rs3025039 polymorphisms by TaqMan assays. Pulmonary function tests were collected from all the patients. VEGF serum levels were determined by ELISA in a subgroup of patients. No VEGF genotype, allele, carrier, or haplotype differences were found between ILD patients and controls as well as between IIP and non-IIP patients. However, an association of rs1570360 with IIP in women and also with lung function in IIP patients was found. None of the VEGF polymorphisms were associated with VEGF levels. In conclusion, our results suggest that VEGF does not seem to play a relevant role in ILD, although rs1570360 may influence the severity of ILD in women and a worse outcome in IIP patients. Full article
(This article belongs to the Special Issue Pneumonia Basic Science)
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16 pages, 2279 KiB  
Article
Sex-Dependent Changes in Right Ventricular Gene Expression in Response to Pressure Overload in a Rat Model of Pulmonary Trunk Banding
Biomedicines 2020, 8(10), 430; https://doi.org/10.3390/biomedicines8100430 - 19 Oct 2020
Cited by 3 | Viewed by 2512
Abstract
Right ventricular hypertrophy (RVH) and subsequent failure are consequences of pulmonary arterial hypertension (PAH). While females are four times more likely to develop PAH, male patients have poorer survival even with treatment, suggesting a sex-dependent dimorphism in right ventricular (RV) hypertrophy/compensation. This may [...] Read more.
Right ventricular hypertrophy (RVH) and subsequent failure are consequences of pulmonary arterial hypertension (PAH). While females are four times more likely to develop PAH, male patients have poorer survival even with treatment, suggesting a sex-dependent dimorphism in right ventricular (RV) hypertrophy/compensation. This may result from differential gene expression in the RV in male vs. female. To date, the sex dependent effect of pressure overload on RV function and changes in gene expression is still unclear. We hypothesize that pressure overload promotes gene expression changes in the RV that may contribute to a poorer outcome in males vs. females. To test this hypothesis, male and female Wistar rats underwent either a sham procedure (sham controls) or moderate pulmonary trunk banding (PTB) (a model of pressure overload induced compensated RV hypertrophy) surgery. Seven weeks post-surgery, RV function was assessed in vivo, and tissue samples were collected for gene expression using qPCR. Compared to sham controls, PTB induced significant increases in the right ventricular systolic pressure, the filling pressure and contractility, which were similar between male and female rats. PTB resulted in an increase in RVH indexes (RV weight, RV weight/tibia length and Fulton index) in both male and female groups. However, RVH indexes were significantly higher in male-PTB when compared to female-PTB rats. Whilst end of procedure body weight was greater in male rats, end of procedure pulmonary artery (PA) diameters were the same in both males and females. RV gene expression analysis revealed that the following genes were increased in PTB-male rats compared with the sham-operated controls: natriuretic peptide A (ANP) and B (BNP), as well as the markers of fibrosis; collagen type I and III. In females, only BNP was significantly increased in the RV when compared to the sham-operated female rats. Furthermore, ANP, BNP and collagen III were significantly higher in the RV from PTB-males when compared to RV from PTB-female rats. Our data suggest that pressure overload-mediated changes in gene expression in the RV from male rats may worsen RVH and increase the susceptibility of males to a poorer outcome when compared to females. Full article
(This article belongs to the Special Issue Pneumonia Basic Science)
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20 pages, 1903 KiB  
Review
Mucus, Microbiomes and Pulmonary Disease
Biomedicines 2021, 9(6), 675; https://doi.org/10.3390/biomedicines9060675 - 13 Jun 2021
Cited by 19 | Viewed by 4533
Abstract
The respiratory tract harbors a stable and diverse microbial population within an extracellular mucus layer. Mucus provides a formidable defense against infection and maintaining healthy mucus is essential to normal pulmonary physiology, promoting immune tolerance and facilitating a healthy, commensal lung microbiome that [...] Read more.
The respiratory tract harbors a stable and diverse microbial population within an extracellular mucus layer. Mucus provides a formidable defense against infection and maintaining healthy mucus is essential to normal pulmonary physiology, promoting immune tolerance and facilitating a healthy, commensal lung microbiome that can be altered in association with chronic respiratory disease. How one maintains a specialized (healthy) microbiome that resists significant fluctuation remains unknown, although smoking, diet, antimicrobial therapy, and infection have all been observed to influence microbial lung homeostasis. In this review, we outline the specific role of polymerizing mucin, a key functional component of the mucus layer that changes during pulmonary disease. We discuss strategies by which mucin feed and spatial orientation directly influence microbial behavior and highlight how a compromised mucus layer gives rise to inflammation and microbial dysbiosis. This emerging field of respiratory research provides fresh opportunities to examine mucus, and its function as predictors of infection risk or disease progression and severity across a range of chronic pulmonary disease states and consider new perspectives in the development of mucolytic treatments. Full article
(This article belongs to the Special Issue Pneumonia Basic Science)
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14 pages, 289 KiB  
Review
Interstitial Pneumonia with Autoimmune Features: Why Rheumatologist-Pulmonologist Collaboration Is Essential
Biomedicines 2021, 9(1), 17; https://doi.org/10.3390/biomedicines9010017 - 26 Dec 2020
Cited by 12 | Viewed by 3240
Abstract
In 2015 the European Respiratory Society (ERS) and the American Thoracic Society (ATS) “Task Force on Undifferentiated Forms of Connective Tissue Disease-associated Interstitial Lung Disease” proposed classification criteria for a new research category defined as “Interstitial Pneumonia with Autoimmune Features” (IPAF), to uniformly [...] Read more.
In 2015 the European Respiratory Society (ERS) and the American Thoracic Society (ATS) “Task Force on Undifferentiated Forms of Connective Tissue Disease-associated Interstitial Lung Disease” proposed classification criteria for a new research category defined as “Interstitial Pneumonia with Autoimmune Features” (IPAF), to uniformly define patients with interstitial lung disease (ILD) and features of autoimmunity, without a definite connective tissue disease. These classification criteria were based on a variable combination of features obtained from three domains: a clinical domain consisting of extra-thoracic features, a serologic domain with specific autoantibodies, and a morphologic domain with imaging patterns, histopathological findings, or multicompartment involvement. Features suggesting a systemic vasculitis were excluded. Since publication of ERS/ATS IPAF research criteria, various retrospective studies have been published focusing on prevalence; clinical, morphological, and serological features; and prognosis of these patients showing a broad heterogeneity in the results. Recently, two prospective, cohort studies were performed, confirming the existence of some peculiarities for this clinical entity and the possible progression of IPAF to a defined connective tissue disease (CTD) in about 15% of cases. Moreover, a non-specific interstitial pneumonia pattern, an anti-nuclear antibody positivity, and a Raynaud phenomenon were the most common findings. In comparison with idiopathic pulmonary fibrosis (IPF), IPAF patients showed a better performance in pulmonary function tests and less necessity of oxygen delivery. However, at this stage of our knowledge, we believe that further prospective studies, possibly derived from multicenter cohorts and through randomized control trials, to further validate the proposed classification criteria are needed. Full article
(This article belongs to the Special Issue Pneumonia Basic Science)
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