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Omics in Infectious Pulmonary Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 5794

Special Issue Editor


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Guest Editor
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Internal Medicine, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Republic of Korea
Interests: host-pathogen interactions; biomarkers; omics; metagenome; tuberculosis; pneumonia; Covid-19; lung diseases

Special Issue Information

Dear Colleagues,

Infectious lung disease is a global health problem and could be a threat to the world because it could spread rapidly. The progression and severity of pulmonary infectious disease is decided by host defense mechanism and virulence of pathogen. To understand the pathogenesis and treatment traits for infectious pulmonary diseases, omics studies including genomics, transcriptomics, metabolomics, proteomics and epigenetics could provide insights to better understanding of diseases and to innovative treatment modalities. This Special Issue is focused on omics studies for various infectious pulmonary diseases for diagnosis, pathogenesis, and treatment against the pathogen itself and the interaction and environment between the host and pathogens.

Dr. Jee Youn Oh
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. Current Issues in Molecular Biology is an international peer-reviewed open access monthly 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 2200 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

  • mycobacterial disease
  • tuberculosis, pneumonia
  • bronchiectasis
  • Covid-19
  • pulmonary diseases
  • covid-19
  • metagenome
  • NGS
  • transcriptomics
  • metabolomics
  • proteomics
  • epigenetics

Published Papers (2 papers)

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Research

8 pages, 410 KiB  
Article
COVID-19 Survivor Patients Carrying the Rs35705950 Risk Allele in MUC5B Have Higher Plasma Levels of Mucin 5B
by Salvador García-Carmona, Ramcés Falfán-Valencia, Abigail Verónica-Aguilar, Ivette Buendía-Roldán, Leslie Chávez-Galán, Rafael de Jesús Hernández-Zenteno, Alfonso Martínez-Morales, Ingrid Fricke-Galindo, Jesús Alanis-Ponce, Daniela Valencia-Pérez Rea, Ilse Adriana Gutiérrez-Pérez, Oscar Zaragoza-García, Karol J. Nava-Quiroz, Angel Camarena, Mayra Mejía, Iris Paola Guzmán-Guzmán and Gloria Pérez-Rubio
Curr. Issues Mol. Biol. 2022, 44(8), 3283-3290; https://doi.org/10.3390/cimb44080226 - 22 Jul 2022
Cited by 5 | Viewed by 2178
Abstract
Background: Genetic susceptibility to infectious diseases is partly due to the variation in the human genome, and COVID-19 is not the exception. This study aimed to identify whether risk alleles of known genes linked with emphysema (SERPINA1) and pulmonary fibrosis ( [...] Read more.
Background: Genetic susceptibility to infectious diseases is partly due to the variation in the human genome, and COVID-19 is not the exception. This study aimed to identify whether risk alleles of known genes linked with emphysema (SERPINA1) and pulmonary fibrosis (MUC5B) are associated with severe COVID-19, and whether plasma mucin 5B differs according to patients’ outcomes. Materials and methods: We included 1258 Mexican subjects diagnosed with COVID-19. We genotyped rs2892474 and rs17580 of the SERPINA1 gene and rs35705950 of MUC5B. Based on the rs35705950 genotypes, mucin 5B plasma protein levels were quantified. Results: Homozygous for the risk alleles of the three polymorphisms were found in less than 5% of the study population, but no statistically significant difference in the genotype or allele association analysis. At the protein level, non-survivors carrying one or two copies of the risk allele rs35705950 in MUC5B (GT + TT) had lower levels of mucin 5B compared to the survivors (0.0 vs. 0.17 ng/mL, p = 0.0013). Conclusion: The polymorphisms rs28929474 and rs17580 of SERPINA1 and rs35705950 of MUC5B are not associated with the risk of severe COVID-19 in the Mexican population. COVID-19 survivor patients bearing one or two copies of the rs35705950 risk allele have higher plasma levels of mucin 5B. Full article
(This article belongs to the Special Issue Omics in Infectious Pulmonary Diseases)
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17 pages, 2418 KiB  
Article
Investigating the Link between Alpha-1 Antitrypsin and Human Neutrophil Elastase in Bronchoalveolar Lavage Fluid of COVID-19 Patients
by Maura D’Amato, Valentina Vertui, Laura Pandolfi, Sara Bozzini, Tommaso Fossali, Riccardo Colombo, Anna Aliberti, Marco Fumagalli, Paolo Iadarola, Camilla Didò, Simona Viglio and Federica Meloni
Curr. Issues Mol. Biol. 2022, 44(5), 2122-2138; https://doi.org/10.3390/cimb44050143 - 10 May 2022
Cited by 6 | Viewed by 3114
Abstract
Neutrophils play a pathogenic role in COVID-19 by releasing Neutrophils Extracellular Traps (NETs) or human neutrophil elastase (HNE). Given that HNE is inhibited by α1-antitrypsin (AAT), we aimed to assess the content of HNE, α1-antitrypsin (AAT) and HNE–AAT complexes (the AAT/HNE balance) in [...] Read more.
Neutrophils play a pathogenic role in COVID-19 by releasing Neutrophils Extracellular Traps (NETs) or human neutrophil elastase (HNE). Given that HNE is inhibited by α1-antitrypsin (AAT), we aimed to assess the content of HNE, α1-antitrypsin (AAT) and HNE–AAT complexes (the AAT/HNE balance) in 33 bronchoalveolar lavage fluid (BALf) samples from COVID-19 patients. These samples were submitted for Gel-Electrophoresis, Western Blot and ELISA, and proteins (bound to AAT or HNE) were identified by Liquid Chromatography-Mass Spectrometry. NETs’ release was analyzed by confocal microscopy. Both HNE and AAT were clearly detectable in BALf at high levels. Contrary to what was previously observed in other settings, the formation of HNE–AAT complex was not detected in COVID-19. Rather, HNE was found to be bound to acute phase proteins, histones and C3. Due to the relevant role of NETs, we assessed the ability of free AAT to bind to histones. While confirming this binding, AAT was not able to inhibit NET formation. In conclusion, despite the finding of a high burden of free and bound HNE, the lack of the HNE–AAT inhibitory complex in COVID-19 BALf demonstrates that AAT is not able to block HNE activity. Furthermore, while binding to histones, AAT does not prevent NET formation nor their noxious activity. Full article
(This article belongs to the Special Issue Omics in Infectious Pulmonary Diseases)
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