Macrophages, Inflammation and Lung Disease
A special issue of Bioengineering (ISSN 2306-5354).
Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 5988
Special Issue Editors
Interests: macrophage; innate immunity; pulmonary fibrosis; chronic lung disease
Special Issues, Collections and Topics in MDPI journals
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
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