The Epithelial-Immune Crosstalk in Pulmonary Fibrosis

Interactions between the lung epithelium and the immune system involve a tight regulation to prevent inappropriate reactions and have been connected to several pulmonary diseases. Although the distal lung epithelium and local immunity have been implicated in the pathogenesis and disease course of id...

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Main Authors: Thomas Planté-Bordeneuve, Charles Pilette, Antoine Froidure
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-05-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2021.631235/full
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author Thomas Planté-Bordeneuve
Charles Pilette
Charles Pilette
Antoine Froidure
Antoine Froidure
author_facet Thomas Planté-Bordeneuve
Charles Pilette
Charles Pilette
Antoine Froidure
Antoine Froidure
author_sort Thomas Planté-Bordeneuve
collection DOAJ
description Interactions between the lung epithelium and the immune system involve a tight regulation to prevent inappropriate reactions and have been connected to several pulmonary diseases. Although the distal lung epithelium and local immunity have been implicated in the pathogenesis and disease course of idiopathic pulmonary fibrosis (IPF), consequences of their abnormal interplay remain less well known. Recent data suggests a two-way process, as illustrated by the influence of epithelial-derived periplakin on the immune landscape or the effect of macrophage-derived IL-17B on epithelial cells. Additionally, damage associated molecular patterns (DAMPs), released by damaged or dying (epithelial) cells, are augmented in IPF. Next to “sterile inflammation”, pathogen-associated molecular patterns (PAMPs) are increased in IPF and have been linked with lung fibrosis, while outer membrane vesicles from bacteria are able to influence epithelial-macrophage crosstalk. Finally, the advent of high-throughput technologies such as microbiome-sequencing has allowed for the identification of a disease-specific microbial environment. In this review, we propose to discuss how the interplays between the altered distal airway and alveolar epithelium, the lung microbiome and immune cells may shape a pro-fibrotic environment. More specifically, it will highlight DAMPs-PAMPs pathways and the specificities of the IPF lung microbiome while discussing recent elements suggesting abnormal mucosal immunity in pulmonary fibrosis.
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spelling doaj.art-73c4f827d40845878691b4e0c2a559c92022-12-21T18:52:23ZengFrontiers Media S.A.Frontiers in Immunology1664-32242021-05-011210.3389/fimmu.2021.631235631235The Epithelial-Immune Crosstalk in Pulmonary FibrosisThomas Planté-Bordeneuve0Charles Pilette1Charles Pilette2Antoine Froidure3Antoine Froidure4Pôle de pneumologie, O.R.L. et dermatologie, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Bruxelles, BelgiumPôle de pneumologie, O.R.L. et dermatologie, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Bruxelles, BelgiumService de pneumologie, Cliniques universitaires Saint-Luc, Bruxelles, BelgiumPôle de pneumologie, O.R.L. et dermatologie, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Bruxelles, BelgiumService de pneumologie, Cliniques universitaires Saint-Luc, Bruxelles, BelgiumInteractions between the lung epithelium and the immune system involve a tight regulation to prevent inappropriate reactions and have been connected to several pulmonary diseases. Although the distal lung epithelium and local immunity have been implicated in the pathogenesis and disease course of idiopathic pulmonary fibrosis (IPF), consequences of their abnormal interplay remain less well known. Recent data suggests a two-way process, as illustrated by the influence of epithelial-derived periplakin on the immune landscape or the effect of macrophage-derived IL-17B on epithelial cells. Additionally, damage associated molecular patterns (DAMPs), released by damaged or dying (epithelial) cells, are augmented in IPF. Next to “sterile inflammation”, pathogen-associated molecular patterns (PAMPs) are increased in IPF and have been linked with lung fibrosis, while outer membrane vesicles from bacteria are able to influence epithelial-macrophage crosstalk. Finally, the advent of high-throughput technologies such as microbiome-sequencing has allowed for the identification of a disease-specific microbial environment. In this review, we propose to discuss how the interplays between the altered distal airway and alveolar epithelium, the lung microbiome and immune cells may shape a pro-fibrotic environment. More specifically, it will highlight DAMPs-PAMPs pathways and the specificities of the IPF lung microbiome while discussing recent elements suggesting abnormal mucosal immunity in pulmonary fibrosis.https://www.frontiersin.org/articles/10.3389/fimmu.2021.631235/fulllung fibrosismucosal immunityepitheliummucusinnate immunity
spellingShingle Thomas Planté-Bordeneuve
Charles Pilette
Charles Pilette
Antoine Froidure
Antoine Froidure
The Epithelial-Immune Crosstalk in Pulmonary Fibrosis
Frontiers in Immunology
lung fibrosis
mucosal immunity
epithelium
mucus
innate immunity
title The Epithelial-Immune Crosstalk in Pulmonary Fibrosis
title_full The Epithelial-Immune Crosstalk in Pulmonary Fibrosis
title_fullStr The Epithelial-Immune Crosstalk in Pulmonary Fibrosis
title_full_unstemmed The Epithelial-Immune Crosstalk in Pulmonary Fibrosis
title_short The Epithelial-Immune Crosstalk in Pulmonary Fibrosis
title_sort epithelial immune crosstalk in pulmonary fibrosis
topic lung fibrosis
mucosal immunity
epithelium
mucus
innate immunity
url https://www.frontiersin.org/articles/10.3389/fimmu.2021.631235/full
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