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Biomedicines
Special Issues
The Molecular Basis of the Immune Response in Pulmonary Fibrosis
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The Molecular Basis of the Immune Response in Pulmonary Fibrosis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1246

Special Issue Editors

Dr. Tamara Cruz

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Guest Editor
Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain
Interests: immunology; pulmonary fibrosis; aging; senescence
Dr. Fernanda Hernandez

E-Mail
Guest Editor
Department of Respiratory Medicine, Respiratory Institute, Hospital Clinic Barcelona, 08036 Barcelona, Spain
Interests: immunology; pulmonary fibrosis; aging; senescence

Special Issue Information

Dear Colleagues,

Different molecular mechanisms have been associated with the development and progression of pulmonary fibrosis. Environmental chronic exposures induce repetitive microinjuries that cause an aberrant activation of the epithelial cells. There is an abnormal repair, mediated by the proliferation of fibroblasts, its activation into myofibroblasts, and the production of large amounts of extracellular matrix components. In addition, as an age-associated disease, there is an accumulation of senescent cells with a very active cytokine and extracellular matrix production. In this complex scenario, the lung immune response is a double-edged sword. While excess inflammation can result in further tissue damage and promote the fibrotic process, defects of immune surveillance and immune resolution allow for the accumulation of fibrosis and senescent cells. This Special Issue of Biomedicines aims to focus on recent advances identifying molecular mechanisms affecting the immune response in the fibrotic lung.

Dr. Tamara Cruz
Dr. Fernanda Hernandez
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. Biomedicines 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 2600 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

  • immune response
  • fibrosis
  • aging
  • senescence

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Published Papers (1 paper)

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Research

16 pages, 4239 KiB  
Article
Caveolin Scaffolding Domain (CSD) Peptide LTI-2355 Modulates the Phagocytic and Synthetic Activity of Lung-Derived Myeloid Cells in Idiopathic Pulmonary Fibrosis (IPF) and Post-Acute Sequelae of COVID Fibrosis (PASC-F)
by Brecht Creyns, BreAnne MacKenzie, Yago Amigo Pinho Jannini Sa, Ana Lucia Coelho, Dale Christensen, Tanyalak Parimon, Brian Windsor and Cory M. Hogaboam
Biomedicines 2025, 13(4), 796; https://doi.org/10.3390/biomedicines13040796 - 26 Mar 2025
Viewed by 960
Abstract
Rationale: The role of the innate immune system in idiopathic pulmonary fibrosis (IPF) remains poorly understood. However, a functional myeloid compartment is required to remove dying cells and cellular debris, as well as to mediate innate immune responses against pathogens. Aberrant macrophage [...] Read more.
Rationale: The role of the innate immune system in idiopathic pulmonary fibrosis (IPF) remains poorly understood. However, a functional myeloid compartment is required to remove dying cells and cellular debris, as well as to mediate innate immune responses against pathogens. Aberrant macrophage activity has been described in patients with post-acute sequelae of COVID fibrosis (PASC-F), and caveolin scaffolding domain (CSD) peptides have been found to attenuate inflammation and fibrosis in mouse lung injury models. Therefore, we examined, for the first time, the effects of CSD peptide LTI-2355 on the functional and synthetic properties of human myeloid cells isolated from lung explant tissue of donor lungs as well as IPF and PASC-F lung explant tissue. Methods and Results: CD45+ myeloid cells isolated from lung explant tissue from IPF and PASC-F patients exhibited an impaired capacity to clear autologous dead cells and cellular debris. The uptake of pathogen-coated bioparticles was impaired in myeloid cells from both fibrotic patient groups independent of the type of pathogen, highlighting an intrinsic functional cell impairment. LTI-2355 improved the phagocytic activity of both IPF and PASC-F myeloid cells, and this improvement was paired with decreased proinflammatory and pro-fibrotic synthetic activity. LTI-2355 was also shown to primarily target CD206-expressing IPF and PASC-F myeloid cells. Conclusions: Primary myeloid cells from IPF and PASC-F patients exhibit dysfunctional phagocytic and synthetic properties that are modulated by LTI-2355. LTI-2355 treatment of IPF myeloid cells resulted in significantly reduced sCD163, IFN-α2, IFN-γ, IL-2, IL-10, IL-12p40, and MMP-1 in the cell supernatant. This study highlights an additional mechanism of action of the CSD peptide in the treatment of IPF and progressive fibrotic lung disease. Full article
(This article belongs to the Special Issue The Molecular Basis of the Immune Response in Pulmonary Fibrosis)
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