The alpha-melanocyte-stimulating hormone acts as a local immune homeostasis factor in experimental allergic asthma.


Journal

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
ISSN: 1365-2222
Titre abrégé: Clin Exp Allergy
Pays: England
ID NLM: 8906443

Informations de publication

Date de publication:
07 2019
Historique:
received: 30 11 2018
revised: 01 03 2019
accepted: 23 03 2019
pubmed: 14 4 2019
medline: 21 8 2020
entrez: 14 4 2019
Statut: ppublish

Résumé

Originally, the neuropeptide α-melanocyte-stimulating hormone (α-MSH) has been described as a mediator of skin pigmentation. However, recent studies have shown that α-MSH is able to modulate inflammation in various tissues including the lung. So far, it is still not clear whether α-MSH also plays a role in allergic bronchial asthma. This study aimed at investigating the role and regulatory mechanisms of α-MSH in asthma pathogenesis. α-MSH levels were measured in bronchoalveolar lavage (BAL) fluid of asthmatic and non-asthmatic individuals as well as of healthy mice and mice with experimental asthma. Wild-type mice were sensitized to ovalbumin (OVA) and exposed to an OVA aerosol in order to induce experimental allergic asthma. α-MSH was administrated intratracheally, the α-MSH antibody intraperitoneally prior each OVA challenge. Airway inflammation, cytokine production, mucus production, airway hyperresponsiveness and receptor expression were assessed. α-MSH levels in BAL of asthmatic individuals and mice were significantly higher compared to healthy controls. In a mouse model of experimental asthma, α-MSH neutralization increased airway inflammation and mucus production, whereas local administration of α-MSH significantly reduced inflammation of the airways. The beneficial effects were further associated with decreased levels of eosinophilic chemoattractant factors that are released by MC5R-positive T helper 2 and airway epithelial cells. α-MSH acts as a regulatory factor to maintain local immune homeostasis in allergic bronchial asthma.

Sections du résumé

BACKGROUND
Originally, the neuropeptide α-melanocyte-stimulating hormone (α-MSH) has been described as a mediator of skin pigmentation. However, recent studies have shown that α-MSH is able to modulate inflammation in various tissues including the lung. So far, it is still not clear whether α-MSH also plays a role in allergic bronchial asthma.
OBJECTIVE
This study aimed at investigating the role and regulatory mechanisms of α-MSH in asthma pathogenesis.
METHODS
α-MSH levels were measured in bronchoalveolar lavage (BAL) fluid of asthmatic and non-asthmatic individuals as well as of healthy mice and mice with experimental asthma. Wild-type mice were sensitized to ovalbumin (OVA) and exposed to an OVA aerosol in order to induce experimental allergic asthma. α-MSH was administrated intratracheally, the α-MSH antibody intraperitoneally prior each OVA challenge. Airway inflammation, cytokine production, mucus production, airway hyperresponsiveness and receptor expression were assessed.
RESULTS
α-MSH levels in BAL of asthmatic individuals and mice were significantly higher compared to healthy controls. In a mouse model of experimental asthma, α-MSH neutralization increased airway inflammation and mucus production, whereas local administration of α-MSH significantly reduced inflammation of the airways. The beneficial effects were further associated with decreased levels of eosinophilic chemoattractant factors that are released by MC5R-positive T helper 2 and airway epithelial cells.
CONCLUSION AND CLINICAL RELEVANCE
α-MSH acts as a regulatory factor to maintain local immune homeostasis in allergic bronchial asthma.

Identifiants

pubmed: 30980429
doi: 10.1111/cea.13400
doi:

Substances chimiques

alpha-MSH 581-05-5

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1026-1039

Informations de copyright

© 2019 John Wiley & Sons Ltd.

Auteurs

Sina Webering (S)

Division of Asthma Exacerbation & Regulation, Priority Area Asthma & Allergy, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

Lars Peter Lunding (LP)

Division of Asthma Exacerbation & Regulation, Priority Area Asthma & Allergy, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

Christina Vock (C)

Division of Experimental Pneumology, Priority Area Asthma & Allergy, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

Alexandra Schröder (A)

Division of Asthma Exacerbation & Regulation, Priority Area Asthma & Allergy, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

Karoline I Gaede (KI)

BioMaterialBank Nord, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

Christian Herzmann (C)

Center for Clinical Studies, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

Heinz Fehrenbach (H)

Division of Experimental Pneumology, Priority Area Asthma & Allergy, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

Michael Wegmann (M)

Division of Asthma Exacerbation & Regulation, Priority Area Asthma & Allergy, Research Center Borstel- Leibniz Lung Center, Borstel, Germany.

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Classifications MeSH