Osteopontin protects against pneumococcal infection in a murine model of allergic airway inflammation.


Journal

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

Informations de publication

Date de publication:
04 2019
Historique:
received: 21 06 2018
revised: 17 08 2018
accepted: 07 09 2018
pubmed: 27 10 2018
medline: 6 5 2020
entrez: 27 10 2018
Statut: ppublish

Résumé

In atopic asthma, chronic Th2-biased inflammation is associated with an increased risk of pneumococcal infection. The anionic phosphoglycoprotein osteopontin (OPN) is highly expressed in asthma and has been ascribed several roles during inflammation. This study aimed to investigate whether OPN affects inflammation and vulnerability to pneumococcal infection in atopic asthma. House dust mite (HDM) extract was used to induce allergic airway inflammation in both wild-type (Spp1 Both allergen challenge in individuals with allergic asthma and the intranasal instillation of HDM in mice resulted in increased OPN levels in bronchoalveolar lavage fluid (BALF). More immune cells (including alveolar macrophages, neutrophils, eosinophils, and lymphocytes) and higher levels of proinflammatory cytokines were found in Spp1 OPN reduces inflammation, decreases tissue injury, and reduces bacterial loads during concurrent pneumococcal infection and allergic airway inflammation in a murine model. These findings suggest that OPN significantly affects vulnerability to pneumococcal infection in atopic asthma.

Sections du résumé

BACKGROUND
In atopic asthma, chronic Th2-biased inflammation is associated with an increased risk of pneumococcal infection. The anionic phosphoglycoprotein osteopontin (OPN) is highly expressed in asthma and has been ascribed several roles during inflammation. This study aimed to investigate whether OPN affects inflammation and vulnerability to pneumococcal infection in atopic asthma.
METHODS
House dust mite (HDM) extract was used to induce allergic airway inflammation in both wild-type (Spp1
RESULTS
Both allergen challenge in individuals with allergic asthma and the intranasal instillation of HDM in mice resulted in increased OPN levels in bronchoalveolar lavage fluid (BALF). More immune cells (including alveolar macrophages, neutrophils, eosinophils, and lymphocytes) and higher levels of proinflammatory cytokines were found in Spp1
CONCLUSION
OPN reduces inflammation, decreases tissue injury, and reduces bacterial loads during concurrent pneumococcal infection and allergic airway inflammation in a murine model. These findings suggest that OPN significantly affects vulnerability to pneumococcal infection in atopic asthma.

Identifiants

pubmed: 30362569
doi: 10.1111/all.13646
doi:

Substances chimiques

Protective Agents 0
Spp1 protein, mouse 0
Osteopontin 106441-73-0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

663-674

Subventions

Organisme : Swedish Heart and Lung Foundation
Pays : International
Organisme : Swedish Government Funds for Clinical Research (ALF)
Pays : International
Organisme : Swedish Foundation for Strategic Research
Pays : International
Organisme : Åke Wiberg Foundation
Pays : International
Organisme : Alfred Österlund Foundation
Pays : International
Organisme : Swedish Research Council
Pays : International

Informations de copyright

© 2018 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.

Auteurs

Gopinath Kasetty (G)

Department of Clinical Sciences Lund, Respiratory Medicine & Allergology, Skåne University Hospital, Lund University, Lund, Sweden.

Ravi K V Bhongir (RKV)

Department of Clinical Sciences Lund, Respiratory Medicine & Allergology, Skåne University Hospital, Lund University, Lund, Sweden.

Praveen Papareddy (P)

Infection Medicine, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden.

Ellen Tufvesson (E)

Department of Clinical Sciences Lund, Respiratory Medicine & Allergology, Skåne University Hospital, Lund University, Lund, Sweden.

Henning Stenberg (H)

Department of Clinical Sciences Lund, Respiratory Medicine & Allergology, Skåne University Hospital, Lund University, Lund, Sweden.

Leif Bjermer (L)

Department of Clinical Sciences Lund, Respiratory Medicine & Allergology, Skåne University Hospital, Lund University, Lund, Sweden.

Anna Hultgårdh-Nilsson (A)

Department of Experimental Medical Science, Lund University, Lund, Sweden.

Heiko Herwald (H)

Infection Medicine, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden.

Arne Egesten (A)

Department of Clinical Sciences Lund, Respiratory Medicine & Allergology, Skåne University Hospital, Lund University, Lund, Sweden.

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Classifications MeSH