Special Issue "Biomarkers in Lung Diseases: From Pathogenesis to Prediction of New Therapies"

A special issue of Journal of Respiration (ISSN 2673-527X).

Deadline for manuscript submissions: closed (15 October 2021).

Special Issue Editors

Dr. Miriana d'Alessandro
E-Mail Website
Guest Editor
Respiratory Diseases and Lung Transplant Unit, Department of Medical and Surgical Sciences and Neurosciences, University of Siena, 53100 Siena, Italy
Interests: pulmonary fibrosis; immunology; lung transplantation; sarcoidosis; rare interstitial lung diseases; biological markers
Special Issues, Collections and Topics in MDPI journals
Dr. Laura Bergantini
E-Mail Website
Guest Editor
Respiratory Diseases and Lung Transplant Unit, Department of Medical and Surgical Sciences & Neurosciences, University of Siena, 53100 Siena, Italy
Interests: severe asthma; immunology; idiopathic pulmonary fibrosis; sarcoidosis; lung transplantation; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Several pathologies affect the lungs and airways, including inflammation, infection and fibrosis. Alteration of angiogenesis, coagulation, fibrogenesis and tissue repair, as well as epithelial damage, matrix remodelling and oxidative stress, are implicated in several lung diseases’ pathogenesis. Biomarkers are measurable indicators that can evaluate pathological biological processes, and they can be categorised by the following major mechanistic pathways: (1) alveolar epithelial cell damage; (2) aberrant fibrogenesis, fibroproliferation and matrix remodelling; (3) immune dysregulation; (4) vascular and endothelial damage; and (5) morphological biomarkers including chest CT scan and genetics. However, disease-specific biomarkers are lacking, and large longitudinal studies are needed before the translational use of the potential biomarkers in clinical practice. Despite the sustained research efforts during the last years focused on the identification of biomarkers applicable in clinical practice for the management of lung diseases, their utility in diagnosis, prognosis and therapy is still controversial. In the era of personalized medicine, it is important to be able to phenotype the disease and to define biomarkers able to elucidate the pathogenesis and to provide new target therapies.

Dr. Miriana d'Alessandro
Dr. Laura Bergantini
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 papers will be 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. Journal of Respiration is an international peer-reviewed open access quarterly 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 1000 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

  • biomarkers
  • pulmonary fibrosis
  • therapies
  • interstitial lung diseases
  • asthma

Published Papers (1 paper)

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

Research

Communication
Immune Correlates of Non-Necrotic and Necrotic Granulomas in Pulmonary Tuberculosis: A Pilot Study
J. Respir. 2021, 1(4), 248-259; https://0-doi-org.brum.beds.ac.uk/10.3390/jor1040023 - 29 Oct 2021
Viewed by 230
Abstract
A granuloma, a pathologic hallmark of tuberculosis (TB), is a complex cellular structure that develops at the site of Mycobacterium tuberculosis (Mtb) infection and is comprised of different immune cell types. Severe pulmonary TB in humans is characterized by the presence of heterogeneous [...] Read more.
A granuloma, a pathologic hallmark of tuberculosis (TB), is a complex cellular structure that develops at the site of Mycobacterium tuberculosis (Mtb) infection and is comprised of different immune cell types. Severe pulmonary TB in humans is characterized by the presence of heterogeneous granulomas, ranging from highly cellular to solid/non-necrotic and necrotic lesions, within the lungs. The host-Mtb interactions within the granulomas dictate the containment of Mtb infection or its progression into a necrotic, cavitary disease. However, the immune environment in various granulomas is poorly understood. The myeloid-derived suppressor cells (MDSCs) are key immune cells that regulate the protective versus permissive host responses against Mtb infection. However, their contexture within the lung granulomas remains unclear. In this study, using single and multiplex immunohistochemical staining, we analyzed the distribution of MDSCs, macrophages, CD4+ T cells and their immunometabolic and effector function states in the solid/non-necrotic and necrotic granulomas in patients with active pulmonary TB. We found increased MDSCs with elevated expression of immunosuppressive molecules in the solid/non-necrotic granulomas. In contrast, cells in the solid and necrotic granulomas produced similar levels of IL-6 and IL-10. Our findings suggest that MDSCs are present in solid/non-necrotic granuloma, which may play an essential role in the progression into a necrotic lesion, thus exacerbating disease pathology and transmission. Full article
Show Figures

Figure 1

Back to TopTop