Contents
Special Issue Topic

Lung Fibrosis—Models and Mechanisms

Submission Deadline: June 30, 2025

Guest Editor

Prof. Bernhard Ryffel E-Mail

Professor, INEM, UMR7355, CNRS, University of Orleans, Orleans, France

Research Keywords: Mechanisms of inflammation, innate immune danger sensing, inflammasome activation, IL-33 and Th17/Th22 differentiation

About the Special lssue

The lung is a critical organ for gas exchange and overall health. Chronic environmental exposures may cause injury to the respiratory barrier, leading to inflammation, emphysema, and progressive interstitial fibrosis, ultimately resulting in respiratory failure. This special issue will begin with an overview of human fibrotic diseases and then address the following key topics:

  • Aerosol and systemic exposure to particles, smoke, allergens, chemicals, ozone, radiation, as well as viral, bacterial, parasitic, and helminth infections.

  • Clinical perspectives on COPD, including rodent and in vitro models, and their predictive value for COPD.

  • Idiopathic pulmonary fibrosis (IPF) and preclinical models.

  • Molecular mechanisms of fibrosis progression and cell death pathways.

  • The role of TLR, inflammasomes, DNA sensing, and cross-talk between pathways.

  • Inflammaging, senescence, and autophagy.

  • Inflammatory cytokines such as TNF and IL-1 family members, and growth factors.

  • The contribution of intestinal microbiota and metabolism, including SCFA, tryptophan, and serotonin.

  • Prevention and therapy: new therapeutic targets and drug candidates.

Keywords: TNF, IL-1, growth factors, NLRP, TLR, autophagy, senescence, pollution, microbiome, metabolites, disease models

Published Articles

Open Access Review
The role of pulmonary vascular endothelium in chronic obstructive pulmonary disease (COPD): Does endothelium play a role in the onset and progression of COPD?
Chronic obstructive pulmonary disease (COPD) is an inflammatory lung pathology characterized by persistent airflow limitation and is the third leading cause of death globally. COPD pathophysiology i
Published: December 29, 2023 Explor Med. 2023;4:1116–1134
3537 109 2
Open Access Review
Mechanism of lungs fibrosis in mycobacterial infection
Lung tuberculosis (TB) remains a heavy burden on public health worldwide. This review discusses mainly the mechanisms of the development of pulmonary fibrosis in an experimental TB model in mice. Th
Published: December 12, 2023 Explor Med. 2023;4:956–976
4519 67 0
Open Access Perspective
Utility of fibroblasts derived from broncho-alveolar lavage of patients with idiopathic pulmonary fibrosis or related disorders to develop in vitro models
Broncho-alveolar lavage (BAL) represents a safe tool for the differential diagnosis of various pulmonary fibrotic diseases. Idiopathic pulmonary fibrosis (IPF) belongs to a heterogeneous group of di
Published: August 31, 2023 Explor Med. 2023;4:461–470
1704 22 0
Open Access Original Article
Mechanistic approaching study in COVID-19 patients treated with high doses of vitamin D
Aim: To evaluate angiotensin II (Ang II) and Ang-(1-7) levels and the cytokine profile in patients hospitalized with mild coronavirus disease 2019 (COVID-19) and contrast them with patients with identical clinical conditions but treated with high doses of vitamin D (vitD). Methods: From the 218 patients recruited (ClinicalTrials.gov NCT04411446), 16 participated in this sub-study and were randomized to a single oral dose of 500,000 IU vitD (n = 10) or placebo (n = 6). Plasmatic Ang II and Ang-(1-7) levels were determined by radioimmunoassay and interleukins (ILs) 1, 6, 8, and 10 and tumor necrosis factor alpha (TNF-α) by enzyme-linked immunosorbent assay before and after treatment. Parallel, serum 25-hydroxyvitamin D3 (25-OH vitD) concentrations as vitD status was measured by a chemiluminescence immunoassay. Results: A trend towards an increase in Ang-(1-7) and a decrease in Ang II levels were observed in placebo- and vitD-treated COVID-19 patients compared to baseline values. There was no difference in Ang II and Ang-(1-7) levels between placebo- and vitD-treated COVID-19 patients. Similar results were obtained with ILs profile. COVID-19 patients showed an increase in the protective component of the RAS which was not improved by vitD treatment. Conclusions: VitD did not improve RAS disbalance in COVID-19. Notwithstanding, the authors visualize that acute treatment with high doses of vitD may show a trend to a decline in inflammatory ILs and an increase in protective markers. Finally, the authors would like to highlight the limitations of this preliminary study, namely the small number of patients and the use of a large single bolus dose of vitD rather than lower daily doses for extended periods with prolonged follow-up times. All these factors need special consideration in the designs of new vitD supplementation trials. All these factors need special consideration in the designs of new vitD supplementation trials (ClinicalTrials.gov identifier: NCT04411446).
Published: April 26, 2023 Explor Med. 2023;4:246–253
1593 30 1