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Regulatory T Cells Limit Pneumococcus-Induced Exacerbation of Lung Fibrosis in Mice

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Regulatory T Cells Limit Pneumococcus-Induced Exacerbation of Lung Fibrosis in Mice. / Moyé, Steffi; Bormann, Tina; Maus, Regina; Sparwasser, Tim; Sandrock, Inga; Prinz, Immo; Warnecke, Gregor; Welte, Tobias; Gauldie, Jack; Kolb, Martin; Maus, Ulrich A.

In: J IMMUNOL, Vol. 204, No. 9, 01.05.2020, p. 2429-2438.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Moyé, S, Bormann, T, Maus, R, Sparwasser, T, Sandrock, I, Prinz, I, Warnecke, G, Welte, T, Gauldie, J, Kolb, M & Maus, UA 2020, 'Regulatory T Cells Limit Pneumococcus-Induced Exacerbation of Lung Fibrosis in Mice', J IMMUNOL, vol. 204, no. 9, pp. 2429-2438. https://doi.org/10.4049/jimmunol.1900980

APA

Moyé, S., Bormann, T., Maus, R., Sparwasser, T., Sandrock, I., Prinz, I., Warnecke, G., Welte, T., Gauldie, J., Kolb, M., & Maus, U. A. (2020). Regulatory T Cells Limit Pneumococcus-Induced Exacerbation of Lung Fibrosis in Mice. J IMMUNOL, 204(9), 2429-2438. https://doi.org/10.4049/jimmunol.1900980

Vancouver

Moyé S, Bormann T, Maus R, Sparwasser T, Sandrock I, Prinz I et al. Regulatory T Cells Limit Pneumococcus-Induced Exacerbation of Lung Fibrosis in Mice. J IMMUNOL. 2020 May 1;204(9):2429-2438. https://doi.org/10.4049/jimmunol.1900980

Bibtex

@article{beec7e88761f4e8b975ec5cae993c3dd,
title = "Regulatory T Cells Limit Pneumococcus-Induced Exacerbation of Lung Fibrosis in Mice",
abstract = "Patients with idiopathic pulmonary fibrosis (IPF) can experience life-threatening episodes of acute worsening of their disease, termed acute exacerbation of IPF, which may be caused by bacterial and/or viral infections. The potential for regulatory T cells (Tregs) to limit disease progression in bacterially triggered fibrosis exacerbation has not been explored so far. In the current study, we show that the number of Tregs was significantly increased in mice with established AdTGF-β1-induced lung fibrosis and further increased in mice with pneumococcal infection-induced lung fibrosis exacerbation. Diphtheria toxin-induced depletion of Tregs significantly worsened infection-induced fibrosis exacerbation as determined by increased lung collagen deposition, lung histology, and elevated pulmonary Th1/Th2 cytokine levels. Conversely, IL-2 complex-induced Treg expansion in wild-type mice with established lung fibrosis completely inhibited pneumococcal infection-induced fibrosis exacerbation as efficaciously as antibiotic treatment while preserving lung antibacterial immunity in mice. Collectively, these findings demonstrate the efficacy of Tregs as {"}silencers,{"} suppressing infection-induced exacerbation of lung fibrosis in mice, and their expansion may offer a novel adjunctive treatment to limit acute exacerbations in patients with IPF.",
keywords = "Animals, Cytokines/immunology, Disease Models, Animal, Disease Progression, Female, Idiopathic Pulmonary Fibrosis/immunology, Interleukin-2/immunology, Lung/immunology, Male, Mice, Mice, Inbred C57BL, Pneumococcal Infections/immunology, Streptococcus pneumoniae/immunology, T-Lymphocytes, Regulatory/immunology, Th1 Cells/immunology, Th17 Cells/immunology",
author = "Steffi Moy{\'e} and Tina Bormann and Regina Maus and Tim Sparwasser and Inga Sandrock and Immo Prinz and Gregor Warnecke and Tobias Welte and Jack Gauldie and Martin Kolb and Maus, {Ulrich A}",
note = "Copyright {\textcopyright} 2020 by The American Association of Immunologists, Inc.",
year = "2020",
month = may,
day = "1",
doi = "10.4049/jimmunol.1900980",
language = "English",
volume = "204",
pages = "2429--2438",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "9",

}

RIS

TY - JOUR

T1 - Regulatory T Cells Limit Pneumococcus-Induced Exacerbation of Lung Fibrosis in Mice

AU - Moyé, Steffi

AU - Bormann, Tina

AU - Maus, Regina

AU - Sparwasser, Tim

AU - Sandrock, Inga

AU - Prinz, Immo

AU - Warnecke, Gregor

AU - Welte, Tobias

AU - Gauldie, Jack

AU - Kolb, Martin

AU - Maus, Ulrich A

N1 - Copyright © 2020 by The American Association of Immunologists, Inc.

PY - 2020/5/1

Y1 - 2020/5/1

N2 - Patients with idiopathic pulmonary fibrosis (IPF) can experience life-threatening episodes of acute worsening of their disease, termed acute exacerbation of IPF, which may be caused by bacterial and/or viral infections. The potential for regulatory T cells (Tregs) to limit disease progression in bacterially triggered fibrosis exacerbation has not been explored so far. In the current study, we show that the number of Tregs was significantly increased in mice with established AdTGF-β1-induced lung fibrosis and further increased in mice with pneumococcal infection-induced lung fibrosis exacerbation. Diphtheria toxin-induced depletion of Tregs significantly worsened infection-induced fibrosis exacerbation as determined by increased lung collagen deposition, lung histology, and elevated pulmonary Th1/Th2 cytokine levels. Conversely, IL-2 complex-induced Treg expansion in wild-type mice with established lung fibrosis completely inhibited pneumococcal infection-induced fibrosis exacerbation as efficaciously as antibiotic treatment while preserving lung antibacterial immunity in mice. Collectively, these findings demonstrate the efficacy of Tregs as "silencers," suppressing infection-induced exacerbation of lung fibrosis in mice, and their expansion may offer a novel adjunctive treatment to limit acute exacerbations in patients with IPF.

AB - Patients with idiopathic pulmonary fibrosis (IPF) can experience life-threatening episodes of acute worsening of their disease, termed acute exacerbation of IPF, which may be caused by bacterial and/or viral infections. The potential for regulatory T cells (Tregs) to limit disease progression in bacterially triggered fibrosis exacerbation has not been explored so far. In the current study, we show that the number of Tregs was significantly increased in mice with established AdTGF-β1-induced lung fibrosis and further increased in mice with pneumococcal infection-induced lung fibrosis exacerbation. Diphtheria toxin-induced depletion of Tregs significantly worsened infection-induced fibrosis exacerbation as determined by increased lung collagen deposition, lung histology, and elevated pulmonary Th1/Th2 cytokine levels. Conversely, IL-2 complex-induced Treg expansion in wild-type mice with established lung fibrosis completely inhibited pneumococcal infection-induced fibrosis exacerbation as efficaciously as antibiotic treatment while preserving lung antibacterial immunity in mice. Collectively, these findings demonstrate the efficacy of Tregs as "silencers," suppressing infection-induced exacerbation of lung fibrosis in mice, and their expansion may offer a novel adjunctive treatment to limit acute exacerbations in patients with IPF.

KW - Animals

KW - Cytokines/immunology

KW - Disease Models, Animal

KW - Disease Progression

KW - Female

KW - Idiopathic Pulmonary Fibrosis/immunology

KW - Interleukin-2/immunology

KW - Lung/immunology

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Pneumococcal Infections/immunology

KW - Streptococcus pneumoniae/immunology

KW - T-Lymphocytes, Regulatory/immunology

KW - Th1 Cells/immunology

KW - Th17 Cells/immunology

U2 - 10.4049/jimmunol.1900980

DO - 10.4049/jimmunol.1900980

M3 - SCORING: Journal article

C2 - 32213566

VL - 204

SP - 2429

EP - 2438

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 9

ER -