Interleukin-11 signaling underlies fibrosis, parenchymal dysfunction, and chronic inflammation of the airway.
Exp Mol Med
; 52(12): 1871-1878, 2020 12.
Artículo
en Inglés
| MEDLINE | ID: covidwho-1012677
ABSTRACT
Interleukin (IL)-11 evolved as part of the innate immune response. In the human lung, IL-11 upregulation has been associated with viral infections and a range of fibroinflammatory diseases, including idiopathic pulmonary fibrosis. Transforming growth factor-beta (TGFß) and other disease factors can initiate an autocrine loop of IL-11 signaling in pulmonary fibroblasts, which, in a largely ERK-dependent manner, triggers the translation of profibrotic proteins. Lung epithelial cells also express the IL-11 receptor and transition into a mesenchymal-like state in response to IL-11 exposure. In mice, therapeutic targeting of IL-11 with antibodies can arrest and reverse bleomycin-induced pulmonary fibrosis and inflammation. Intriguingly, fibroblast-specific blockade of IL-11 signaling has anti-inflammatory effects, which suggests that lung inflammation is sustained, in part, through IL-11 activity in the stroma. Proinflammatory fibroblasts and their interaction with the damaged epithelium may represent an important but overlooked driver of lung disease. Initially thought of as a protective cytokine, IL-11 is now increasingly recognized as an important determinant of lung fibrosis, inflammation, and epithelial dysfunction.
Texto completo:
Disponible
Colección:
Bases de datos internacionales
Base de datos:
MEDLINE
Asunto principal:
Enfermedades Respiratorias
/
Transducción de Señal
/
Interleucina-11
/
Inflamación
Tipo de estudio:
Estudios diagnósticos
/
Estudio pronóstico
Límite:
Animales
/
Humanos
Idioma:
Inglés
Revista:
Exp Mol Med
Asunto de la revista:
Biologia Molecular
/
Bioquímica
Año:
2020
Tipo del documento:
Artículo
País de afiliación:
S12276-020-00531-5
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