Interleukin-22 regulates interferon lambda expression in a mice model of pseudomonas aeruginosa pneumonia

Alexis Broquet; Anissa Besbes; Jérôme Martin; Cédric Jacqueline; Mickaël Vourc'h; Antoine Roquilly; Jocelyne Caillon; Régis Josien; Karim Asehnoune

doi:10.1016/j.molimm.2019.12.003

Interleukin-22 regulates interferon lambda expression in a mice model of pseudomonas aeruginosa pneumonia

Alexis Broquet
, Anissa Besbes
, Jérôme Martin
, Cédric Jacqueline
, Mickaël Vourc'h
, Antoine Roquilly
, Jocelyne Caillon
, Régis Josien
, Karim Asehnoune

Research output: Contribution to journal › Article › peer-review

20 Scopus citations

Abstract

Background: Interleukin (IL)-22 is a cytokine involved in tissue protection and repair following lung pathologies. Interferon (IFN)-λ cytokines displayed similar properties during viral infection and a synergy of action between these two players has been documented in the intestine. We hypothesize that during Pseudomonas aeruginosa challenge, IL-22 up-regulates IFN-λ and that IFN-λ exhibits protective functions during Pseudomonas aeruginosa acute pneumonia model in mice. Methods: Using an in vitro human alveolar epithelial cell line A549, we assessed the ability of IL-22 to enhance IFN-λ expression during infection. IFN-λ protective function was evaluated in an acute mouse pneumonia model. Results: We first demonstrated in murine lungs that only type-II alveolar cells express IL-22 receptor and that IL-22 treatment of A549 cell line up-regulates IFN-λ expression. In a murine acute pneumonia model, IL-22 administration maintained significant IFN-λ levels in the broncho-alveolar fluids whereas IL-22 neutralization abolished IFN-λ up-regulation. In vivo administration of IFN-λ during Pseudomonas aeruginosa pneumonia improves mice outcome by dampening neutrophil recruitment and decreasing epithelium damages. Discussion: We show here that IL-22 regulates IFN-λ levels during Pseudomonas aeruginosa pneumonia.

Original language	English
Pages (from-to)	52-59
Number of pages	8
Journal	Molecular Immunology
Volume	118
DOIs	https://doi.org/10.1016/j.molimm.2019.12.003
State	Published - Feb 2020
Externally published	Yes

Keywords

Alveolar epithelial cells
Host response
Interferon-λ
Interleukin-22
Neutrophils
Pseudomonas aeruginosa

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10.1016/j.molimm.2019.12.003

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title = "Interleukin-22 regulates interferon lambda expression in a mice model of pseudomonas aeruginosa pneumonia",

abstract = "Background: Interleukin (IL)-22 is a cytokine involved in tissue protection and repair following lung pathologies. Interferon (IFN)-λ cytokines displayed similar properties during viral infection and a synergy of action between these two players has been documented in the intestine. We hypothesize that during Pseudomonas aeruginosa challenge, IL-22 up-regulates IFN-λ and that IFN-λ exhibits protective functions during Pseudomonas aeruginosa acute pneumonia model in mice. Methods: Using an in vitro human alveolar epithelial cell line A549, we assessed the ability of IL-22 to enhance IFN-λ expression during infection. IFN-λ protective function was evaluated in an acute mouse pneumonia model. Results: We first demonstrated in murine lungs that only type-II alveolar cells express IL-22 receptor and that IL-22 treatment of A549 cell line up-regulates IFN-λ expression. In a murine acute pneumonia model, IL-22 administration maintained significant IFN-λ levels in the broncho-alveolar fluids whereas IL-22 neutralization abolished IFN-λ up-regulation. In vivo administration of IFN-λ during Pseudomonas aeruginosa pneumonia improves mice outcome by dampening neutrophil recruitment and decreasing epithelium damages. Discussion: We show here that IL-22 regulates IFN-λ levels during Pseudomonas aeruginosa pneumonia.",

keywords = "Alveolar epithelial cells, Host response, Interferon-λ, Interleukin-22, Neutrophils, Pseudomonas aeruginosa",

author = "Alexis Broquet and Anissa Besbes and J{\'e}r{\^o}me Martin and C{\'e}dric Jacqueline and Micka{\"e}l Vourc'h and Antoine Roquilly and Jocelyne Caillon and R{\'e}gis Josien and Karim Asehnoune",

note = "Publisher Copyright: {\textcopyright} 2019",

year = "2020",

month = feb,

doi = "10.1016/j.molimm.2019.12.003",

language = "English",

volume = "118",

pages = "52--59",

journal = "Molecular Immunology",

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TY - JOUR

T1 - Interleukin-22 regulates interferon lambda expression in a mice model of pseudomonas aeruginosa pneumonia

AU - Broquet, Alexis

AU - Besbes, Anissa

AU - Martin, Jérôme

AU - Jacqueline, Cédric

AU - Vourc'h, Mickaël

AU - Roquilly, Antoine

AU - Caillon, Jocelyne

AU - Josien, Régis

AU - Asehnoune, Karim

PY - 2020/2

Y1 - 2020/2

N2 - Background: Interleukin (IL)-22 is a cytokine involved in tissue protection and repair following lung pathologies. Interferon (IFN)-λ cytokines displayed similar properties during viral infection and a synergy of action between these two players has been documented in the intestine. We hypothesize that during Pseudomonas aeruginosa challenge, IL-22 up-regulates IFN-λ and that IFN-λ exhibits protective functions during Pseudomonas aeruginosa acute pneumonia model in mice. Methods: Using an in vitro human alveolar epithelial cell line A549, we assessed the ability of IL-22 to enhance IFN-λ expression during infection. IFN-λ protective function was evaluated in an acute mouse pneumonia model. Results: We first demonstrated in murine lungs that only type-II alveolar cells express IL-22 receptor and that IL-22 treatment of A549 cell line up-regulates IFN-λ expression. In a murine acute pneumonia model, IL-22 administration maintained significant IFN-λ levels in the broncho-alveolar fluids whereas IL-22 neutralization abolished IFN-λ up-regulation. In vivo administration of IFN-λ during Pseudomonas aeruginosa pneumonia improves mice outcome by dampening neutrophil recruitment and decreasing epithelium damages. Discussion: We show here that IL-22 regulates IFN-λ levels during Pseudomonas aeruginosa pneumonia.

AB - Background: Interleukin (IL)-22 is a cytokine involved in tissue protection and repair following lung pathologies. Interferon (IFN)-λ cytokines displayed similar properties during viral infection and a synergy of action between these two players has been documented in the intestine. We hypothesize that during Pseudomonas aeruginosa challenge, IL-22 up-regulates IFN-λ and that IFN-λ exhibits protective functions during Pseudomonas aeruginosa acute pneumonia model in mice. Methods: Using an in vitro human alveolar epithelial cell line A549, we assessed the ability of IL-22 to enhance IFN-λ expression during infection. IFN-λ protective function was evaluated in an acute mouse pneumonia model. Results: We first demonstrated in murine lungs that only type-II alveolar cells express IL-22 receptor and that IL-22 treatment of A549 cell line up-regulates IFN-λ expression. In a murine acute pneumonia model, IL-22 administration maintained significant IFN-λ levels in the broncho-alveolar fluids whereas IL-22 neutralization abolished IFN-λ up-regulation. In vivo administration of IFN-λ during Pseudomonas aeruginosa pneumonia improves mice outcome by dampening neutrophil recruitment and decreasing epithelium damages. Discussion: We show here that IL-22 regulates IFN-λ levels during Pseudomonas aeruginosa pneumonia.

KW - Alveolar epithelial cells

KW - Host response

KW - Interferon-λ

KW - Interleukin-22

KW - Neutrophils

KW - Pseudomonas aeruginosa

UR - https://www.scopus.com/pages/publications/85076356315

U2 - 10.1016/j.molimm.2019.12.003

DO - 10.1016/j.molimm.2019.12.003

M3 - Article

C2 - 31855807

AN - SCOPUS:85076356315

SN - 0161-5890

VL - 118

SP - 52

EP - 59

JO - Molecular Immunology

JF - Molecular Immunology

ER -

Interleukin-22 regulates interferon lambda expression in a mice model of pseudomonas aeruginosa pneumonia

Abstract

Keywords

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