Pulmonary Fibrosis and Cell Therapy

Topic Information

Dear Colleagues,

During these last two decades, cell therapies for the treatment of pulmonary fibrosis have been considered a promising treatment. In that time, different types of stem cells or lung progenitor cells have been evaluated, mostly in animal models and only in a few human clinical trials. However, although both preclinical and human clinical data support the safety of cell therapies, they have not been translated into routine clinical practice. The reasons are diverse, since many key unanswered questions remain, such as doubts about the type of cells to be transplanted, the origin of these cells (autologous or heterologous), the route of administration (intravenous or endotracheal), the dose, the best time for transplantation, and others. Additionally, the concern about side effects, such as unwanted differentiation of the grafted stem cells, cannot be ignored. In addition to answering these questions, it is essential to know the mechanisms by which cell therapies exert their positive effects. Recent studies indicate that most positive effects can be attributed to the cellular secretome, composed of free soluble proteins and extracellular vesicles. The use of the secretome would avoid the side effects associated with cells, as well as the difficulty in obtaining and expanding them. Therefore, it is not only important to answer these questions, but also to know the mechanisms by which cell therapies exert their positive effects. All of this knowledge would help to consolidate cell therapies in clinical practice. This Topic aims to summarize the updated knowledge on different cell therapies and the mechanisms involved in their potential therapeutic effect in pulmonary fibrosis. The Topic, entitled “Pulmonary Fibrosis and Cell Therapy”, will include both review and original research papers covering key topics related to different cell therapies for pulmonary fibrosis, such as:
(1) different types of stem cells, induced pluripotent stem cells (iPSC), non-derived and derived from pulmonary cells;
(2) lung progenitor cells;
(3) other type of pulmonary cells;
(4) the cell secretome;
(5) cell–cell interactions;
(6) investigation of mechanisms of lung tissue regeneration, cell engraftment, or the cell secretome.

We hope that our readers from various disciplines will benefit from this Topic, which will serve as a gateway to the amazing world of cell therapies for fibrotic diseases. We look forward to your contributions.

Dr. Victor Ivo Peinado
Dr. Anna Serrano-Mollar
Dr. Olga Tura-Ceide
Topic Editors

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomolecules biomolecules	5.5	8.3	2011	16.9 Days	CHF 2700
Cells cells	6.0	9.0	2012	16.6 Days	CHF 2700
International Journal of Molecular Sciences ijms	5.6	7.8	2000	16.3 Days	CHF 2900
Journal of Molecular Pathology jmp	-	-	2020	24.9 Days	CHF 1000
Organoids organoids	-	-	2022	15.0 days *	CHF 1000

* Median value for all MDPI journals in the second half of 2023.

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Published Papers (1 paper)

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Open AccessArticle

Invadosome Formation by Lung Fibroblasts in Idiopathic Pulmonary Fibrosis

by Mégane Lebel, Dominic O. Cliche, Martine Charbonneau, Damien Adam, Emmanuelle Brochiero, Claire M. Dubois and André M. Cantin

Int. J. Mol. Sci. 2023, 24(1), 499; https://doi.org/10.3390/ijms24010499 - 28 Dec 2022

Cited by 2 | Viewed by 2291

Abstract

Idiopathic pulmonary fibrosis (IPF) is characterized by abnormal fibroblast accumulation in the lung leading to extracellular matrix deposition and remodeling that compromise lung function. However, the mechanisms of interstitial invasion and remodeling by lung fibroblasts remain poorly understood. The invadosomes, initially described in [...] Read more.

Idiopathic pulmonary fibrosis (IPF) is characterized by abnormal fibroblast accumulation in the lung leading to extracellular matrix deposition and remodeling that compromise lung function. However, the mechanisms of interstitial invasion and remodeling by lung fibroblasts remain poorly understood. The invadosomes, initially described in cancer cells, consist of actin-based adhesive structures that coordinate with numerous other proteins to form a membrane protrusion capable of degrading the extracellular matrix to promote their invasive phenotype. In this regard, we hypothesized that invadosome formation may be increased in lung fibroblasts from patients with IPF. Public RNAseq datasets from control and IPF lung tissues were used to identify differentially expressed genes associated with invadosomes. Lung fibroblasts isolated from bleomycin-exposed mice and IPF patients were seeded with and without the two approved drugs for treating IPF, nintedanib or pirfenidone on fluorescent gelatin-coated coverslips for invadosome assays. Several matrix and invadosome-associated genes were increased in IPF tissues and in IPF fibroblastic foci. Invadosome formation was significantly increased in lung fibroblasts isolated from bleomycin-exposed mice and IPF patients. The degree of lung fibrosis found in IPF tissues correlated strongly with invadosome production by neighboring cells. Nintedanib suppressed IPF and PDGF-activated lung fibroblast invadosome formation, an event associated with inhibition of the PDGFR/PI3K/Akt pathway and TKS5 expression. Fibroblasts derived from IPF lung tissues express a pro-invadosomal phenotype, which correlates with the severity of fibrosis and is responsive to antifibrotic treatment. Full article

(This article belongs to the Topic Pulmonary Fibrosis and Cell Therapy)

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