ijms-logo

Journal Browser

Journal Browser

Acute Lung Injury – New Insights into the Mechanisms and Emerging Therapies 3.0

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

Deadline for manuscript submissions: closed (20 August 2021) | Viewed by 2618

Special Issue Editor


E-Mail Website
Guest Editor
Department of Cellular and Molecular Biology, University of Texas Health Science Center, Tyler, TX 75708, USA
Interests: inflammation; pro-inflammatory cells; mediators of inflammation; innate immunity; cell signaling; signal transduction; lung disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute lung injury (ALI) and its more severe form, termed acute respiratory distress syndrome (ARDS), are complex clinical syndromes associated with uncontrolled systemic inflammatory response. Resulting microvascular damage prompts a substantial increase in both pulmonary vascular and epithelial permeability. Subsequently, airspaces become flooded with protein-rich edema fluid, leading to acute respiratory failure. The causes of ALI include pulmonary and extrapulmonary infections and serious conditions such as sepsis, pancreatitis, trauma, pneumonia, and aspiration. ALI and ARDS affect approximately 150,000 people in the United States each year, and the mortality of more severe cases remains at 30–50%. Current therapies are primarily supportive and focus on treatment of the underlying condition along with mechanical ventilation and corticosteroid administration. Most of the research into ALI pathogenesis and treatment has evolved around identifying causative and prognostically important biomarkers. The underlying objective has been to find mediators responsible for the development of ALI and progression to ARDS, with the ultimate goal of facilitating the diagnosis of ALI in patients before onset of ARDS. However, prognosis of ALI and ARDS has, so far, only witnessed modest improvements which were almost exclusively based on better supportive care.

This Special Issue of the International Journal of Molecular Sciences will focus on recent developments in the area of ALI pathogenesis and treatment, including new insights into the mechanisms of and emerging therapies for ALI and ARDS. It will cover a selection of recent research topics and current review articles in the field of ALI and ARDS. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Prof. Anna K. Kurdowska
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

  • acute lung injury (ALI)
  • acute respiratory distress syndrome (ARDS)
  • inflammation
  • biomarkers
  • molecular pathway
  • therapeutics

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

16 pages, 5255 KiB  
Article
The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced by Coxsackievirus A2 Infection in Mice
by Wangquan Ji, Qiang Hu, Mengdi Zhang, Chuwen Zhang, Chen Chen, Yujie Yan, Xue Zhang, Shuaiyin Chen, Ling Tao, Weiguo Zhang, Yuefei Jin and Guangcai Duan
Int. J. Mol. Sci. 2021, 22(18), 9895; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189895 - 13 Sep 2021
Cited by 7 | Viewed by 2212
Abstract
Sporadic occurrences and outbreaks of hand, foot, and mouth disease (HFMD) caused by Coxsackievirus A2 (CVA2) have frequently reported worldwide recently, which pose a great challenge to public health. Epidemiological studies have suggested that the main cause of death in critical patients is [...] Read more.
Sporadic occurrences and outbreaks of hand, foot, and mouth disease (HFMD) caused by Coxsackievirus A2 (CVA2) have frequently reported worldwide recently, which pose a great challenge to public health. Epidemiological studies have suggested that the main cause of death in critical patients is pulmonary edema. However, the pathogenesis of this underlying comorbidity remains unclear. In this study, we utilized the 5-day-old BALB/c mouse model of lethal CVA2 infection to evaluate lung damage. We found that the permeability of lung microvascular was significantly increased after CVA2 infection. We also observed the direct infection and apoptosis of lung endothelial cells as well as the destruction of tight junctions between endothelial cells. CVA2 infection led to the degradation of tight junction proteins (e.g., ZO-1, claudin-5, and occludin). The gene transcription levels of von Willebrand factor (vWF), endothelin (ET), thrombomodulin (THBD), granular membrane protein 140 (GMP140), and intercellular cell adhesion molecule-1 (ICAM-1) related to endothelial dysfunction were all significantly increased. Additionally, CVA2 infection induced the increased expression of inflammatory cytokines (IL-6, IL-1β, and MCP-1) and the activation of p38 mitogen-activated protein kinase (MAPK). In conclusion, the disruption of the endothelial barrier contributes to acute lung injury induced by CVA2 infection; targeting p38-MAPK signaling may provide a therapeutic approach for pulmonary edema in critical infections of HFMD. Full article
Show Figures

Figure 1

Back to TopTop