Titre :

Human eosinophil activin A synthesis and mRNA stabilization are induced by the combination of IL-3 plus TNF.

Auteur(s) :

Kelly, Elizabeth A [Auteur]
University of Wisconsin School of Medicine and Public Health
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Johnson, Sean H [Auteur]
University of Wisconsin School of Medicine and Public Health
Liu, Lin Ying [Auteur]
University of Wisconsin School of Medicine and Public Health
Malter, James S [Auteur]
University of Texas Southwestern Medical Center [Dallas]
Burnham, Mandy E [Auteur]
University of Wisconsin School of Medicine and Public Health
Jarjour, Nizar N [Auteur]
University of Wisconsin School of Medicine and Public Health

Titre de la revue :

Immunology and Cell Biology

Nom court de la revue :

Immunol Cell Biol

Numéro :

94

Pagination :

701-8

Date de publication :

2016-08-01

ISSN :

1440-1711

Mot(s)-clé(s) en anglais :

Activins
Adult
Enzyme Activation
Eosinophils
Female
Granulocyte-Macrophage Colony-Stimulating Factor
Humans
Hypersensitivity
Inhibin-beta Subunits
Interleukin-3
Interleukin-5
Kinetics
Male
Middle Aged
Mitogen-Activated Protein Kinases
NF-kappa B
Protein Kinase Inhibitors
RNA Stability
RNA, Messenger
Tumor Necrosis Factor-alpha
Young Adult

Discipline(s) HAL :

Sciences du Vivant [q-bio]

Résumé en anglais : [en]

Eosinophils contribute to immune regulation and wound healing/fibrosis in various diseases, including asthma. Growing appreciation for the role of activin A in such processes led us to hypothesize that eosinophils are a ...
Lire la suite >Eosinophils contribute to immune regulation and wound healing/fibrosis in various diseases, including asthma. Growing appreciation for the role of activin A in such processes led us to hypothesize that eosinophils are a source of this transforming growth factor-ß superfamily member. Tumor necrosis factor-α (TNF) induces activin A by other cell types and is often present at the site of allergic inflammation along with the eosinophil-activating common ß (ßc) chain-signaling cytokines (interleukin (IL)-5, IL-3, granulocyte-macrophages colony-stimulating factor (GM-CSF)). Previously, we established that the combination of TNF plus a ßc chain-signaling cytokine synergistically induces eosinophil synthesis of the remodeling enzyme matrix metalloproteinase-9. Therefore, eosinophils were stimulated ex vivo by these cytokines and in vivo through an allergen-induced airway inflammatory response. In contrast to IL-5+TNF or GM-CSF+TNF, the combination of IL-3+TNF synergistically induced activin A synthesis and release by human blood eosinophils. IL-3+TNF enhanced activin A mRNA stability, which required sustained signaling of pathways downstream of p38 and extracellular signal-regulated kinase mitogen-activated protein kinases. In vivo, following segmental airway allergen challenge of subjects with mild allergic asthma, activin A mRNA was upregulated in airway eosinophils compared with circulating eosinophils, and ex vivo, circulating eosinophils tended to release more activin A in response to IL-3+TNF. These data provide evidence that eosinophils release activin A and that this function is enhanced when eosinophils are present in an allergen-induced inflammatory environment. Moreover, these data provide the first evidence for posttranscriptional control of activin A mRNA. We propose that an environment rich in IL-3+TNF will lead to eosinophil-derived activin A, which has an important role in regulating inflammation and/or fibrosis.Lire moins >

Langue :

Anglais

Comité de lecture :

Oui

Audience :

Internationale

Vulgarisation :

Non

Établissement(s) :

Université de Lille
Inserm
CHU Lille

Collections :

• Autres travaux scientifiques

Date de dépôt :

2023-10-23T15:22:28Z
2024-03-18T08:38:33Z