Low oxygen levels decrease adaptive immune responses and ameliorate experimental asthma in mice.


Journal

Allergy
ISSN: 1398-9995
Titre abrégé: Allergy
Pays: Denmark
ID NLM: 7804028

Informations de publication

Date de publication:
03 2022
Historique:
revised: 09 06 2021
received: 12 01 2021
accepted: 13 07 2021
pubmed: 27 7 2021
medline: 9 4 2022
entrez: 26 7 2021
Statut: ppublish

Résumé

High-altitude therapy has been used as add-on treatment for allergic asthma with considerable success. However, the underlying mechanisms remain unclear. In order to investigate the possible therapeutic effects of high-altitude therapy on allergic asthma, we utilized a new in vivo mouse model. Mice were treated with house dust mite (HDM) extract over 4 weeks and co-exposed to 10% oxygen (Hyp) or room air for the final 2 weeks. Experimental asthma was assessed by airway hyper-responsiveness, mucus hypersecretion and inflammatory cell recruitment. Isolated immune cells from mouse and allergic patients were stimulated in vitro with HDM under Hyp and normoxia in different co-culture systems to analyse the adaptive immune response. Compared to HDM-treated mice in room air, HDM-treated Hyp-mice displayed ameliorated mucosal hypersecretion and airway hyper-responsiveness. The attenuated asthma phenotype was associated with strongly reduced activation of antigen-presenting cells (APCs), effector cell infiltration and cytokine secretion. In vitro, hypoxia almost completely suppressed the HDM-induced adaptive immune response in both mouse and human immune cells. While hypoxia did not affect effector T-cell responses per-se, it interfered with antigen-presenting cell (APC) differentiation and APC/effector cell crosstalk. Hypoxia-induced reduction in the Th2-response to HDM ameliorates allergic asthma in vivo. Hypoxia interferes with APC/T-cell crosstalk and confers an unresponsive phenotype to APCs.

Sections du résumé

BACKGROUND
High-altitude therapy has been used as add-on treatment for allergic asthma with considerable success. However, the underlying mechanisms remain unclear. In order to investigate the possible therapeutic effects of high-altitude therapy on allergic asthma, we utilized a new in vivo mouse model.
METHODS
Mice were treated with house dust mite (HDM) extract over 4 weeks and co-exposed to 10% oxygen (Hyp) or room air for the final 2 weeks. Experimental asthma was assessed by airway hyper-responsiveness, mucus hypersecretion and inflammatory cell recruitment. Isolated immune cells from mouse and allergic patients were stimulated in vitro with HDM under Hyp and normoxia in different co-culture systems to analyse the adaptive immune response.
RESULTS
Compared to HDM-treated mice in room air, HDM-treated Hyp-mice displayed ameliorated mucosal hypersecretion and airway hyper-responsiveness. The attenuated asthma phenotype was associated with strongly reduced activation of antigen-presenting cells (APCs), effector cell infiltration and cytokine secretion. In vitro, hypoxia almost completely suppressed the HDM-induced adaptive immune response in both mouse and human immune cells. While hypoxia did not affect effector T-cell responses per-se, it interfered with antigen-presenting cell (APC) differentiation and APC/effector cell crosstalk.
CONCLUSIONS
Hypoxia-induced reduction in the Th2-response to HDM ameliorates allergic asthma in vivo. Hypoxia interferes with APC/T-cell crosstalk and confers an unresponsive phenotype to APCs.

Identifiants

pubmed: 34309864
doi: 10.1111/all.15020
pmc: PMC9290649
doi:

Substances chimiques

Allergens 0
Oxygen S88TT14065

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

870-882

Informations de copyright

© 2021 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.

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Auteurs

Mathias Hochgerner (M)

Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.

Eva M Sturm (EM)

Division of Pharmacology, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.

Diana Schnoegl (D)

Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.

Grazyna Kwapiszewska (G)

Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Division of Physiology, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.

Horst Olschewski (H)

Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Division of Pulmonology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.

Leigh M Marsh (LM)

Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.

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Classifications MeSH