Titre :

La mERA2 des éosinophiles murins aggrave la réponse allergique

Auteur(s) :

Nguyen, Linh Manh [Auteur]
Kanda, Akira [Auteur]
Kamioka, Yuji [Auteur]
Tokuhiro, Keizo [Auteur]
Kobayashi, Yoshiki [Auteur]
Yun, Yasutaka [Auteur]
Bui, Dan Van [Auteur]
Chu, Hanh Hong [Auteur]
Le, Nhi Kieu Thi [Auteur]
Suzuki, Kensuke [Auteur]
Mitani, Akitoshi [Auteur]
Shimamura, Akihiro [Auteur]
Fukui, Kenta [Auteur]
Dombrowicz, David [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Récepteurs Nucléaires, Maladies Métaboliques et Cardiovasculaires - U 1011 [RNMCD]
Iwai, Hiroshi [Auteur]

Titre de la revue :

Allergy

Éditeur :

Wiley

Date de publication :

2024-02-23

ISSN :

0105-4538

Discipline(s) HAL :

Sciences du Vivant [q-bio]

Résumé en anglais : [en]

Background: Eosinophil’s granule cytotoxic proteins, including eosinophil-derived neurotoxin (EDN), have an important role in the pathogenesis of eosinophilic inflammation such as allergic asthma. In the murine, mouse ...
Lire la suite >Background: Eosinophil’s granule cytotoxic proteins, including eosinophil-derived neurotoxin (EDN), have an important role in the pathogenesis of eosinophilic inflammation such as allergic asthma. In the murine, mouse eosinophil-associated ribonuclease-2 (mEAR2) was considered as the murine orthologue of human EDN. However, underlying mechanisms of mEAR2 and EDN action in pathological of allergic asthma remains poorly understood.Methods: To investigate the role of mEAR2, Airway Allergic Inflammation (AAI) was induced by house dust mite (HDM) in genetically modified mice in which exon 2 in the mEAR2 was deleted (mEAR2-/-). Airway hyperresponsiveness (AHR), lung histopathological, bronchoalveolar lavage fluid (BALF) analysis, mEAR2 level analysis, total Immunoglobulin E (IgE) levels and cytokines profiling were performed. Sensitized splenocytes and bone marrow derived eosinophils (bmEOS) were co-cultured with or without HDM and TLR2 antibody to investigate IL-4, -5, and -13 level in the supernatant. Results: We found that mEAR2 concentration was significantly increased in the lung tissue from mEAR2+/+ but not mEAR2-/- mice in AAI. In sensitized and challenged mEAR2-/- mice type 2 cytokines and IgE concentrations were significantly decreased. HDM-sensitized bmEOS from mEAR2+/+ but not from mEAR2-/- mice increased type 2 cytokine production by cocultured splenocytes 4and this increase was completely inhibited in the presence of TLR2 antibody.Conclusion: These data suggest that mEAR2 exacerbates pathogenesis of AAI in a TLR2-dependent manner.Lire moins >

Langue :

Anglais

Comité de lecture :

Oui

Audience :

Internationale

Vulgarisation :

Non

Collections :

• Récepteurs nucléaires, Maladies Cardiovasculaires et Diabète (RNMCD) - U1011

Source :

Harvested from HAL