Blocking pannexin1 reduces airway inflammation in a murine model of asthma.

Détails

ID Serval
serval:BIB_657584D87601
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Blocking pannexin1 reduces airway inflammation in a murine model of asthma.
Périodique
American journal of translational research
Auteur(s)
Khan M., Huang Y.A., Kuo C.Y., Lin T., Lu C.H., Chen L.C., Kuo M.L.
ISSN
1943-8141 (Print)
ISSN-L
1943-8141
Statut éditorial
Publié
Date de publication
2020
Peer-reviewed
Oui
Volume
12
Numéro
7
Pages
4074-4083
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
Stressed or injured cells release ATP into the extracellular milieu via the pannexin1 (Panx1) channels, which is the basis of inflammation in a variety of conditions, including allergic lung inflammation. Although the role of Panx1 in mediating inflammation has been well established, the role of its mimetic peptide, <sup>10</sup> Panx1, which inhibits ATP release from Panx1 channels, in allergic asthma remains understudied. The aim of this study was to evaluate the effects of using <sup>10</sup> Panx1 to inhibit Panx1 channel in a murine model of ovalbumin (OVA)-induced asthma. We demonstrate that blockade of Panx1 significantly attenuated goblet cell hyperplasia and inflammatory cell infiltration into the lungs of OVA-sensitized mice. Inhibition of Panx1 also reduced the total and eosinophil cell numbers in the bronchoalveolar lavage fluid (BALF) and reduced expression of CCL11 and CCL2 in lung tissues from mice. Moreover, we detected lower levels of IL-5 and IL-13 in the culture supernatant of OVA-restimulated splenocytes from <sup>10</sup> Panx1-treated mice. Collectively, our findings suggest that Panx1 inhibition of allergen-mediated lung inflammation has the potential to suppress allergic responses in asthma.
Mots-clé
10Panx1, EXtracellular ATP, asthma, chemokine, lung inflammation, pannexin1
Pubmed
Création de la notice
17/08/2020 10:30
Dernière modification de la notice
11/01/2021 10:33
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