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Cells
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Chronic Inflammatory Disease and COVID-19: Possibilities and Challenges?
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Chronic Inflammatory Disease and COVID-19: Possibilities and Challenges?

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 7262

Special Issue Editor

Prof. Dr. Goo-Bo Jeong

E-Mail Website
Guest Editor
Department of Anatomy and Cell Biology, College of Medicine, Gachon University, Incheon, Republic of Korea
Interests: cancer; regenerative medicine; mesenchymal stem cells; extracellular vesicles; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), led to a devastating pandemic in 2020. COVID-19 and SARS-CoV-2 pose a threat to individuals with pre-existing medical complications related to immune responses. The comorbidities associated with SARS-CoV-2 infected persons can put their life at risk. Several chronic inflammatory diseases, including Alzheimer’s disease, asthma, diabetes mellitus type 2, rheumatoid arthritis, ankylosing spondylitis, cancer, and heart disease, contributed significantly to the worsening rates of SARS-CoV-2 infected patient survival.

The salient prerequisites for understanding COVID-19 pathogenesis and the contributory role of inflammatory diseases in patient outcome must be addressed. The COVID-19 pandemic undeniably set the priorities in clinical practice and research (including bench and bedside). Ongoing research and current datasets are not enough to reach any conclusion that perfectly suits the defined role of chronic inflammatory diseases in SARS-CoV-2 infection.

This Special Issue aims to explore the major challenges in understanding the immunopathogenesis and pathophysiological aspect of SARS-CoV-2 infection, with special focus on chronic inflammatory diseases. This issue also aims to explore possible cost-effective and efficient diagnostic and therapeutic tools along with prophylactic strategies. New windows of pharmacological, holistic approaches and immune-based treatments must be explored for efficient treatment of COVID-19 patients. Finally, we are looking for papers on drug discovery and repurposing for the management of chronic inflammatory diseases in the context of COVID-19.

We would be honored to receive robust contributions from eminent experts in the field in order to update the scientific literature with both original research and review articles on this fascinating topic.

Prof. Dr. Goo-Bo Jeong
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • SARS-CoV-2
  • COVID-19
  • chronic inflammatory disease
  • Alzheimer’s disease
  • asthma
  • diabetes mellitus type 2
  • rheumatoid arthritis
  • ankylosing spondylitis
  • cancer and heart disease
  • drug repurposing
  • pharmacological interventions
  • holistic approach

Published Papers (2 papers)

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Review

10 pages, 881 KiB  
Review
Pathophysiology of Pulmonary Fibrosis in the Context of COVID-19 and Implications for Treatment: A Narrative Review
by Son Tran, Andre Ksajikian, Juliana Overbey, Patrick Li and Yong Li
Cells 2022, 11(16), 2489; https://doi.org/10.3390/cells11162489 - 11 Aug 2022
Cited by 14 | Viewed by 3049
Abstract
Pulmonary fibrosis (PF) is a feared outcome of many pulmonary diseases which results in a reduction in lung compliance and capacity. The development of PF is relatively rare, but it can occur secondary to viral pneumonia, especially COVID-19 infection. While COVID-19 infection and [...] Read more.
Pulmonary fibrosis (PF) is a feared outcome of many pulmonary diseases which results in a reduction in lung compliance and capacity. The development of PF is relatively rare, but it can occur secondary to viral pneumonia, especially COVID-19 infection. While COVID-19 infection and its complications are still under investigation, we can look at a similar outbreak in the past to gain better insight as to the expected long-term outcomes of COVID-19 patient lung function. In the current article, we review the literature relative to PF via PubMed. We also performed a literature search for COVID-related pathological changes in the lungs. Finally, the paper was reviewed and summarized based on the studies’ integrity, relative, or power calculations. This article provides a narrative review that endeavors to elucidate the current understanding of the pathophysiological mechanisms underlying PF and therapeutic strategies. We also discussed the potential for preventing progression to the fibrotic state within the context of the COVID-19 pandemic. With the massive scale of the COVID-19 pandemic, we expect there should more instances of PF due to COVID-19 infection. Patients who survive severe COVID-19 infection may suffer from a high incidence of PF. Full article
(This article belongs to the Special Issue Chronic Inflammatory Disease and COVID-19: Possibilities and Challenges?)
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24 pages, 4819 KiB  
Review
Systematic Review of the Common Pathophysiological Mechanisms in COVID-19 and Neurodegeneration: The Role of Bioactive Compounds and Natural Antioxidants
by Kyonghwan Choe, Hyun Young Park, Muhammad Ikram, Hyeon Jin Lee, Tae Ju Park, Rahat Ullah and Myeong Ok Kim
Cells 2022, 11(8), 1298; https://doi.org/10.3390/cells11081298 - 11 Apr 2022
Cited by 18 | Viewed by 3614
Abstract
The novel coronavirus (2019-nCoVCOVID-19) belongs to the Beta coronavirus family, which contains MERS-CoV (Middle East respiratory syndrome coronavirus) and SARS-CoV (severe acute respiratory syndrome coronavirus). SARS-CoV-2 activates the innate immune system, thereby activating the inflammatory mechanism, causing the release of inflammatory cytokines. Moreover, [...] Read more.
The novel coronavirus (2019-nCoVCOVID-19) belongs to the Beta coronavirus family, which contains MERS-CoV (Middle East respiratory syndrome coronavirus) and SARS-CoV (severe acute respiratory syndrome coronavirus). SARS-CoV-2 activates the innate immune system, thereby activating the inflammatory mechanism, causing the release of inflammatory cytokines. Moreover, it has been suggested that COVID-19 may penetrate the central nervous system, and release inflammatory cytokines in the brains, inducing neuroinflammation and neurodegeneration. Several links connect COVID-19 with Alzheimer’s disease (AD), such as elevated oxidative stress, uncontrolled release of the inflammatory cytokines, and mitochondrial apoptosis. There are severe concerns that excessive immune cell activation in COVID-19 may aggravate the neurodegeneration and amyloid-beta pathology of AD. Here, we have collected the evidence, showing the links between the two diseases. The focus has been made to collect the information on the activation of the inflammation, its contributors, and shared therapeutic targets. Furthermore, we have given future perspectives, research gaps, and overlapping pathological bases of the two diseases. Lastly, we have given the short touch to the drugs that have equally shown rescuing effects against both diseases. Although there is limited information available regarding the exact links between COVID-19 and neuroinflammation, we have insight into the pathological contributors of the diseases. Based on the shared pathological features and therapeutic targets, we hypothesize that the activation of the immune system may induce neurological disorders by triggering oxidative stress and neuroinflammation. Full article
(This article belongs to the Special Issue Chronic Inflammatory Disease and COVID-19: Possibilities and Challenges?)
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