Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
6.8
3.9
Journals
Biomedicines
Special Issues
The Molecular Basis of the Immune Response in Pulmonary Fibrosis
share announcement

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: 31 January 2026 | Viewed by 2623

Special Issue Editors

Dr. Tamara Cruz

E-Mail Website
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

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

15 pages, 2428 KB  
Article
Ethylbenzene Exposure and Bronchoalveolar CD4/CD8 T Cells in Hypersensitivity Pneumonitis Development and Clinical Outcome
by Alfredo Minguela, José A. Campillo, María Isabel Aguilar Sanchís, Antonia Baeza Caracena, Francisco Esquembre, Erika M. Novoa-Bolivar, Rosana González-López, Almudena Otalora, Cristina Ortuño-Hernández, Ruth López-Hernández, Lourdes Gimeno, Inmaculada Ruiz-Lorente, Diana Ceballos, Elena Solana-Martínez, Juan Alcántara-Fructuoso, Manuel Muro and José A. Ros
Biomedicines 2025, 13(11), 2611; https://doi.org/10.3390/biomedicines13112611 - 24 Oct 2025
Viewed by 512
Abstract
Background: Hypersensitivity pneumonitis (HP) is an interstitial lung disease (ILD) characterized by inflammation of the lung parenchyma, alveoli and bronchioles induced by inhalation of organic compounds. Bird-related-HP (BRHP) is the most common type of HP, occurring in susceptible people in regular contact with [...] Read more.
Background: Hypersensitivity pneumonitis (HP) is an interstitial lung disease (ILD) characterized by inflammation of the lung parenchyma, alveoli and bronchioles induced by inhalation of organic compounds. Bird-related-HP (BRHP) is the most common type of HP, occurring in susceptible people in regular contact with birds, although a genetic susceptibility is unclear. This study investigates the impact of environmental volatile organic compounds (VOCs) on the development of HP and other pulmonary diseases, and their relationship with pulmonary inflammatory cell composition and patient outcomes. Methods: Geospatial environmental levels of VOCs (benzene, toluene, ethylbenzene, m,p-xylene and o-xylene) in patients’ homes were related to bronchoalveolar lavage (BAL) leukocyte profiles analyzed by flow cytometry of 1515 patients with different lung diseases in the region of Murcia (southeastern Spain). Results: Ethylbenzene levels over the threshold limit of 10 µg/m3 (EB10) were associated with HP (23.9% vs. 15.2%, p < 0.05). A strong association with HP was observed in patients in contact with birds living in areas with EB10 (63.0% vs. 27.4%, p < 0.001). Linear regression analysis showed that age (B = −0.058, p < 0.012), smoking (B = −0.125, p < 0.001), bird contact (B = 0.275, p < 0.001) and EB10 (B = 0.109, p < 0.001) were independent variables associated with HP. In HP patients, BAL CD4/CD8-ratio > 1.5 was associated with shorter overall survival (8.9 years vs. not-reached, p < 0.011), probably due to lower CD8+ T-lymphocyte counts observed in HP fibrotic patients (11.65 ± 2.8% vs. 23.6 ± 2.9%, p = 0.008) and in those who died during follow-up (10.0 ± 1.9% vs. 23.8 ± 2.7%, p = 0.012), suggesting a protective role for CD8+ T cells. Conclusions: High environmental ethylbenzene is strongly associated with BRHP. CD8+ T-lymphocytes could have a protective role in HP, preventing fibrosis and increasing overall survival. Full article
(This article belongs to the Special Issue The Molecular Basis of the Immune Response in Pulmonary Fibrosis)
►▼ Show Figures

Figure 1

16 pages, 4239 KB  
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
Cited by 1 | Viewed by 1619
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)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop