The transition from normal lung anatomy to minimal and established fibrosis in idiopathic pulmonary fibrosis (IPF).


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Apr 2021
Historique:
received: 16 01 2021
revised: 12 03 2021
accepted: 19 03 2021
pubmed: 17 4 2021
medline: 30 11 2021
entrez: 16 4 2021
Statut: ppublish

Résumé

The transition from normal lung anatomy to minimal and established fibrosis is an important feature of the pathology of idiopathic pulmonary fibrosis (IPF). The purpose of this report is to examine the molecular and cellular mechanisms associated with this transition. Pre-operative thoracic Multidetector Computed Tomography (MDCT) scans of patients with severe IPF (n = 9) were used to identify regions of minimal(n = 27) and established fibrosis(n = 27). MDCT, Micro-CT, quantitative histology, and next-generation sequencing were used to compare 24 samples from donor controls (n = 4) to minimal and established fibrosis samples. The present results extended earlier reports about the transition from normal lung anatomy to minimal and established fibrosis by showing that there are activations of TGFBI, T cell co-stimulatory genes, and the down-regulation of inhibitory immune-checkpoint genes compared to controls. The expression patterns of these genes indicated activation of a field immune response, which is further supported by the increased infiltration of inflammatory immune cells dominated by lymphocytes that are capable of forming lymphoid follicles. Moreover, fibrosis pathways, mucin secretion, surfactant, TLRs, and cytokine storm-related genes also participate in the transitions from normal lung anatomy to minimal and established fibrosis. The transition from normal lung anatomy to minimal and established fibrosis is associated with genes that are involved in the tissue repair processes, the activation of immune responses as well as the increased infiltration of CD4, CD8, B cell lymphocytes, and macrophages. These molecular and cellular events correlate with the development of structural abnormality of IPF and probably contribute to its pathogenesis.

Sections du résumé

BACKGROUND BACKGROUND
The transition from normal lung anatomy to minimal and established fibrosis is an important feature of the pathology of idiopathic pulmonary fibrosis (IPF). The purpose of this report is to examine the molecular and cellular mechanisms associated with this transition.
METHODS METHODS
Pre-operative thoracic Multidetector Computed Tomography (MDCT) scans of patients with severe IPF (n = 9) were used to identify regions of minimal(n = 27) and established fibrosis(n = 27). MDCT, Micro-CT, quantitative histology, and next-generation sequencing were used to compare 24 samples from donor controls (n = 4) to minimal and established fibrosis samples.
FINDINGS RESULTS
The present results extended earlier reports about the transition from normal lung anatomy to minimal and established fibrosis by showing that there are activations of TGFBI, T cell co-stimulatory genes, and the down-regulation of inhibitory immune-checkpoint genes compared to controls. The expression patterns of these genes indicated activation of a field immune response, which is further supported by the increased infiltration of inflammatory immune cells dominated by lymphocytes that are capable of forming lymphoid follicles. Moreover, fibrosis pathways, mucin secretion, surfactant, TLRs, and cytokine storm-related genes also participate in the transitions from normal lung anatomy to minimal and established fibrosis.
INTERPRETATION CONCLUSIONS
The transition from normal lung anatomy to minimal and established fibrosis is associated with genes that are involved in the tissue repair processes, the activation of immune responses as well as the increased infiltration of CD4, CD8, B cell lymphocytes, and macrophages. These molecular and cellular events correlate with the development of structural abnormality of IPF and probably contribute to its pathogenesis.

Identifiants

pubmed: 33862585
pii: S2352-3964(21)00118-3
doi: 10.1016/j.ebiom.2021.103325
pmc: PMC8054143
pii:
doi:

Substances chimiques

Biomarkers 0
Inflammation Mediators 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

103325

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest All other authors declare no competing interests.

Auteurs

Feng Xu (F)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada.

Naoya Tanabe (N)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Dragos M Vasilescu (DM)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada.

John E McDonough (JE)

Leuven Lung Transplant Unit, KU Leuven and UZ Gasthuisberg, Leuven, Belgium.

Harvey O Coxson (HO)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada.

Kohei Ikezoe (K)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada.

Daisuke Kinose (D)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada; Division of Respiratory Medicine, Department of Medicine, Shiga University of Medical Science, Shiga, Japan.

Kevin W Ng (KW)

The Francis Crick Institute, London, UK.

Stijn E Verleden (SE)

Laboratory of Respiratory Diseases, BREATHE, Department of CHROMETA, KU Leuven, Leuven, Belgium.

Wim A Wuyts (WA)

Leuven Lung Transplant Unit, KU Leuven and UZ Gasthuisberg, Leuven, Belgium.

Bart M Vanaudenaerde (BM)

Leuven Lung Transplant Unit, KU Leuven and UZ Gasthuisberg, Leuven, Belgium.

Johny Verschakelen (J)

Leuven Lung Transplant Unit, KU Leuven and UZ Gasthuisberg, Leuven, Belgium.

Joel D Cooper (JD)

Division of Thoracic Surgery, University of Pennsylvania, USA.

Marc E Lenburg (ME)

Boston University Medical Center, Boston, MA, USA.

Katrina B Morshead (KB)

Genentech, Inc., South San Francisco, CA, USA.

Alexander R Abbas (AR)

Genentech, Inc., South San Francisco, CA, USA.

Joseph R Arron (JR)

Genentech, Inc., South San Francisco, CA, USA.

Avrum Spira (A)

Boston University Medical Center, Boston, MA, USA.

Tillie-Louise Hackett (TL)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada.

Thomas V Colby (TV)

Department of Pathology and Laboratory Medicine, Mayo Clinic Arizona, USA.

Christopher J Ryerson (CJ)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada; Department of Medicine, The University of British Columbia, Vancouver, Canada.

Raymond T Ng (RT)

Department of Computer Science, The University of British Columbia, Vancouver, Canada.

James C Hogg (JC)

Center for Heart Lung Innovation, The University of British Columbia, Vancouver, Canada.

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Classifications MeSH