A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity

Abstract Lung fibrosis is characterised by the accumulation of extracellular matrix within the lung and is secondary to both known and unknown aetiologies. This accumulation of scar tissue limits gas exchange causing respiratory insufficiency. The pathogenesis of lung fibrosis is poorly understood,...

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Main Authors: Helen I Warheit‐Niemi, Elissa M Hult, Bethany B Moore
Format: Article
Language:English
Published: Wiley 2019-01-01
Series:Clinical & Translational Immunology
Subjects:
Online Access:https://doi.org/10.1002/cti2.1065
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spelling doaj-7b9ad4cbde984f4b8a32d17e1bfd6a742020-11-24T22:05:01ZengWileyClinical & Translational Immunology2050-00682019-01-0186n/an/a10.1002/cti2.1065A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunityHelen I Warheit‐Niemi0Elissa M Hult1Bethany B Moore2Department of Microbiology and Immunology University of Michigan Ann Arbor MI USADepartment of Molecular and Integrative Physiology University of Michigan Ann Arbor MI USADepartment of Microbiology and Immunology University of Michigan Ann Arbor MI USAAbstract Lung fibrosis is characterised by the accumulation of extracellular matrix within the lung and is secondary to both known and unknown aetiologies. This accumulation of scar tissue limits gas exchange causing respiratory insufficiency. The pathogenesis of lung fibrosis is poorly understood, but immunologic‐based treatments have been largely ineffective. Despite this, accumulating evidence suggests that innate immune cells and receptors play important modulatory roles in the initiation and propagation of the disease. Paradoxically, while innate immune signalling may be important for the pathogenesis of fibrosis, there is also evidence to suggest that innate immune function against pathogens may be impaired, leading to dysregulated and/or impaired host defence. This review summarises the evidence for this pathologic two‐way street, highlights new concepts of pathogenesis and recommends future directions for research emphasis.https://doi.org/10.1002/cti2.1065bacteriacollagenhost defencemacrophageneutrophilToll‐like receptors
collection DOAJ
language English
format Article
sources DOAJ
author Helen I Warheit‐Niemi
Elissa M Hult
Bethany B Moore
spellingShingle Helen I Warheit‐Niemi
Elissa M Hult
Bethany B Moore
A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity
Clinical & Translational Immunology
bacteria
collagen
host defence
macrophage
neutrophil
Toll‐like receptors
author_facet Helen I Warheit‐Niemi
Elissa M Hult
Bethany B Moore
author_sort Helen I Warheit‐Niemi
title A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity
title_short A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity
title_full A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity
title_fullStr A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity
title_full_unstemmed A pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity
title_sort pathologic two‐way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity
publisher Wiley
series Clinical & Translational Immunology
issn 2050-0068
publishDate 2019-01-01
description Abstract Lung fibrosis is characterised by the accumulation of extracellular matrix within the lung and is secondary to both known and unknown aetiologies. This accumulation of scar tissue limits gas exchange causing respiratory insufficiency. The pathogenesis of lung fibrosis is poorly understood, but immunologic‐based treatments have been largely ineffective. Despite this, accumulating evidence suggests that innate immune cells and receptors play important modulatory roles in the initiation and propagation of the disease. Paradoxically, while innate immune signalling may be important for the pathogenesis of fibrosis, there is also evidence to suggest that innate immune function against pathogens may be impaired, leading to dysregulated and/or impaired host defence. This review summarises the evidence for this pathologic two‐way street, highlights new concepts of pathogenesis and recommends future directions for research emphasis.
topic bacteria
collagen
host defence
macrophage
neutrophil
Toll‐like receptors
url https://doi.org/10.1002/cti2.1065
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