Disruption in the balance between apolipoprotein A-I and mast cell chymase in chronic hypersensitivity pneumonitis.
Immun Inflamm Dis
; 8(4): 659-671, 2020 12.
Article
em En
| MEDLINE
| ID: mdl-33016012
ABSTRACT
BACKGROUND:
Apolipoprotein A-I (apoA-I) has an antifibrotic effect in idiopathic pulmonary fibrosis. Although pulmonary fibrosis is associated with poor prognosis of patients with hypersensitivity pneumonitis (HP), little is known regarding the role of apoA-I in the pathogenesis of HP.METHODS:
Two-dimensional electrophoresis, immunoblotting, and enzyme-linked immunosorbent assays were performed for the identification and quantification of apoA-I in bronchoalveolar lavage fluid (BALF) from patients with acute and chronic HP. To investigate the degradation of apoA-I, apoA-I was incubated with BALF. Moreover, the role of apoA-I in TGF-ß1-induced epithelial-mesenchymal transition of A549 cells was examined.RESULTS:
The concentration of apoA-I in the BALF was significantly lower in chronic HP (n = 56) compared with acute HP (n = 31). The expression level of apoA-I was also low in the lung tissues of chronic HP. ApoA-I was degraded by BALF from HP patients. The number of chymase-positive mast cells in the alveolar parenchyma was inversely correlated with apoA-I levels in the BALF of chronic HP patients. In vitro experiment using A549 cells, untreated apoA-I inhibited TGF-ß1-induced epithelial-mesenchymal transition, although this trend was not observed in the chymase-treated apoA-I.CONCLUSIONS:
A decrease of apoA-I was associated with the pathogenesis of chronic HP in terms of pulmonary fibrosis and mast cell chymase attenuated the protective effect of apoA-I against pulmonary fibrosis. Furthermore, apoA-I could be a crucial molecule associated with lung fibrogenesis of HP.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Alveolite Alérgica Extrínseca
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Mastócitos
Limite:
Adult
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Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article