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Kynurenine pathway as a modulator of inflammation in COPD and its exacerbations.

Odile Poulain-Godefroy, Mélina Le Roux, Gwenola Kervoaze, Anais Ollivier, Muriel Pichavant, Philippe Gosset
ERJ Open Research 2022 8: 61; DOI: 10.1183/23120541.LSC-2022.61
Odile Poulain-Godefroy
1CIIL - INSERM U1019 - CNRS UMR 9017 Institut Pasteur de Lille, LILLE, France
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  • For correspondence: odile.poulain@pasteur-lille.fr
Mélina Le Roux
1CIIL - INSERM U1019 - CNRS UMR 9017 Institut Pasteur de Lille, LILLE, France
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Gwenola Kervoaze
1CIIL - INSERM U1019 - CNRS UMR 9017 Institut Pasteur de Lille, LILLE, France
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Anais Ollivier
1CIIL - INSERM U1019 - CNRS UMR 9017 Institut Pasteur de Lille, LILLE, France
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Muriel Pichavant
1CIIL - INSERM U1019 - CNRS UMR 9017 Institut Pasteur de Lille, LILLE, France
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Philippe Gosset
1CIIL - INSERM U1019 - CNRS UMR 9017 Institut Pasteur de Lille, LILLE, France
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Abstract

Introduction: Chronic obstructive pulmonary disease (COPD) is an airway chronic inflammatory disorder. The kynurenine pathway (KP), the major route for tryptophan catabolism, is induced by inflammatory stimuli. The first enzyme of the pathway is indoleamine 2,3-dioxygenase (IDO1). Its activation further leads to the generation of biologically active metabolites with pro- or anti-inflammatory properties.

Aims and objectives: Our objective was to determine whether KP is dysregulated in COPD and its exacerbations and therefore could contribute to the impairment of immune response.

Methods: Mice chronically exposed to cigarette smoke (CS), mimicking COPD symptoms, were infected with influenza virus (H1N1). The expression of the different enzymes of KP was analyzed in pulmonary extracts by RT-qPCR. Immunohistology of the lung was performed to detect the production of kynurenic and quinolic acids. A human bronchial epithelial cell line BEAS-2B, was incubated with cigarette smoke extract (CSE) and influenza virus particles. The expression of KP enzymes (IDO1, KMO, KYNU) was analyzed by RT-qPCR and correlated with the inflammatory and anti-viral response.

Results: The KP is induced by CS in mice lungs and drastically enhanced by viral infections. Immunohistology demonstrated a production of kynurenic and quinolinic acids in epithelia and infiltrating immune cells. IDO1; KMO and KYNU expression were also observed in infected BEAS-2B and their expression was modulated by CSE exposition.

Conclusion: KP activation occurs in lung, upon exposition to cigarette smoke or viral infection and could contribute to inflammation regulation and therefore could become a target for the development of new therapeutics.

  • Immunology
  • Epithelial cell
  • Animal models

Footnotes

Cite this article as ERJ Open Research 2022; 8: Suppl. 8, 61.

This article was presented at the 2022 ERS Lung Science Conference, in session “Poster Session 2”.

This is an ERS Lung Science Conference abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).

  • Copyright ©the authors 2022
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Kynurenine pathway as a modulator of inflammation in COPD and its exacerbations.
Odile Poulain-Godefroy, Mélina Le Roux, Gwenola Kervoaze, Anais Ollivier, Muriel Pichavant, Philippe Gosset
ERJ Open Research Mar 2022, 8 (suppl 8) 61; DOI: 10.1183/23120541.LSC-2022.61

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Kynurenine pathway as a modulator of inflammation in COPD and its exacerbations.
Odile Poulain-Godefroy, Mélina Le Roux, Gwenola Kervoaze, Anais Ollivier, Muriel Pichavant, Philippe Gosset
ERJ Open Research Mar 2022, 8 (suppl 8) 61; DOI: 10.1183/23120541.LSC-2022.61
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