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Bioengineering
Special Issues
Macrophages, Inflammation and Lung Disease
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Macrophages, Inflammation and Lung Disease

A special issue of Bioengineering (ISSN 2306-5354).

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 4437

Special Issue Editors

Dr. Megan Ballinger

E-Mail Website
Guest Editor
Department of Internal Medicine, The Ohio State University, Columbus, OH 43210, USA
Interests: macrophage; innate immunity; pulmonary fibrosis; chronic lung disease
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Samir Ghadiali

E-Mail Website
Guest Editor
Department of Biomedical Engineering, The Ohio State University, Columbus, OH 43210, USA
Interests: biofluid mechanics; biomedical engineering; mechanobiology; ventilator induced lung injury; microRNA therapeutics

Special Issue Information

Dear Colleagues,

As highlighted by the current pandemic, damage to the lung during infectious disease can lead to significant mortality. In addition, the ability of the lung to recover from injury is critical for survival, and abnormal repair can lead to additional complications, such as fibrosis and increased susceptibility to additional insults. The lung is a dynamic and mechanosensitive organ composed of a variety of structural cells, such as epithelial cells, endothelial cells, and fibroblasts, as well as immunological cells (such as macrophages). During homeostasis, these cells work together to ensure gas exchange and oxygenation. While in the setting of infectious or non-infectious inflammation, the structural and immune cells within the lung microenvironment may either alter injury severity or coordinate appropriate lung repair. Therefore, understanding how these cellular interactions in the dynamic lung microenvironment can influence both health and disease is a critical area of research. This Special Issue on “Macrophage, Inflammation and Lung Disease” will focus on original research papers and comprehensive reviews, addressing the complex cellular and micro-environmental interactions that occur within the lung in the setting of a) normal health; b) acute and chronic lung disease; and c) during lung repair and resolution. Topics of interest for this Special Issue include, but are not limited to, the following:

  • Structural and Immune cell interactions that regulate normal lung physiology;
  • Cellular interactions and their ability to regulate lung injury during disease;
  • Influence of microenvironmental cells on fibroblasts mediated remodeling and repair of the lung following injury/inflammation;
  • Development of novel bioengineering models of lung injury, repair and fibrosis;
  • Role of mechano-memory in regulating cellular signaling pathways in the lung;
  • Investigating the role of lung tissue biomechanical behavior in regulating cellular responses and function;
  • Epigenetic mechanisms of lung repair and regeneration;
  • Bioengineering approaches to understand the role of immunity in lung disease.

Dr. Megan Ballinger
Prof. Dr. Samir Ghadiali
Guest Editors

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. Bioengineering 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 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

  • infection
  • inflammation
  • lung injury
  • lung repair
  • mechanotransduction
  • fibrosis

Published Papers (2 papers)

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16 pages, 4286 KiB  
Article
Functional Blockage of S100A8/A9 Ameliorates Ischemia–Reperfusion Injury in the Lung
by Kentaro Nakata, Mikio Okazaki, Tomohisa Sakaue, Rie Kinoshita, Yuhei Komoda, Dai Shimizu, Haruchika Yamamoto, Shin Tanaka, Ken Suzawa, Kazuhiko Shien, Kentaroh Miyoshi, Hiromasa Yamamoto, Toshiaki Ohara, Seiichiro Sugimoto, Masaomi Yamane, Akihiro Matsukawa, Masakiyo Sakaguchi and Shinichi Toyooka
Bioengineering 2022, 9(11), 673; https://0-doi-org.brum.beds.ac.uk/10.3390/bioengineering9110673 - 10 Nov 2022
Cited by 1 | Viewed by 1766
Abstract
(1) Background: Lung ischemia–reperfusion (IR) injury increases the mortality and morbidity of patients undergoing lung transplantation. The objective of this study was to identify the key initiator of lung IR injury and to evaluate pharmacological therapeutic approaches using a functional inhibitor against the [...] Read more.
(1) Background: Lung ischemia–reperfusion (IR) injury increases the mortality and morbidity of patients undergoing lung transplantation. The objective of this study was to identify the key initiator of lung IR injury and to evaluate pharmacological therapeutic approaches using a functional inhibitor against the identified molecule. (2) Methods: Using a mouse hilar clamp model, the combination of RNA sequencing and histological investigations revealed that neutrophil-derived S100A8/A9 plays a central role in inflammatory reactions during lung IR injury. Mice were assigned to sham and IR groups with or without the injection of anti-S100A8/A9 neutralizing monoclonal antibody (mAb). (3) Results: Anti-S100A8/A9 mAb treatment significantly attenuated plasma S100A8/A9 levels compared with control IgG. As evaluated by oxygenation capacity and neutrophil infiltration, the antibody treatment dramatically ameliorated the IR injury. The gene expression levels of cytokines and chemokines induced by IR injury were significantly reduced by the neutralizing antibody. Furthermore, the antibody treatment significantly reduced TUNEL-positive cells, indicating the presence of apoptotic cells. (4) Conclusions: We identified S100A8/A9 as a novel therapeutic target against lung IR injury. Full article
(This article belongs to the Special Issue Macrophages, Inflammation and Lung Disease)
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Review

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25 pages, 2037 KiB  
Review
Significance of Pulmonary Endothelial Injury and the Role of Cyclooxygenase-2 and Prostanoid Signaling
by Rosa Nickl, Sandra Hauser, Jens Pietzsch and Torsten Richter
Bioengineering 2023, 10(1), 117; https://0-doi-org.brum.beds.ac.uk/10.3390/bioengineering10010117 - 14 Jan 2023
Cited by 1 | Viewed by 2123
Abstract
The endothelium plays a key role in the dynamic balance of hemodynamic, humoral and inflammatory processes in the human body. Its central importance and the resulting therapeutic concepts are the subject of ongoing research efforts and form the basis for the treatment of [...] Read more.
The endothelium plays a key role in the dynamic balance of hemodynamic, humoral and inflammatory processes in the human body. Its central importance and the resulting therapeutic concepts are the subject of ongoing research efforts and form the basis for the treatment of numerous diseases. The pulmonary endothelium is an essential component for the gas exchange in humans. Pulmonary endothelial dysfunction has serious consequences for the oxygenation and the gas exchange in humans with the potential of consecutive multiple organ failure. Therefore, in this review, the dysfunction of the pulmonary endothel due to viral, bacterial, and fungal infections, ventilator-related injury, and aspiration is presented in a medical context. Selected aspects of the interaction of endothelial cells with primarily alveolar macrophages are reviewed in more detail. Elucidation of underlying causes and mechanisms of damage and repair may lead to new therapeutic approaches. Specific emphasis is placed on the processes leading to the induction of cyclooxygenase-2 and downstream prostanoid-based signaling pathways associated with this enzyme. Full article
(This article belongs to the Special Issue Macrophages, Inflammation and Lung Disease)
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