Disruption in the balance between apolipoprotein A-I and mast cell chymase in chronic hypersensitivity pneumonitis.
apolipoprotein A-I
chymase
hypersensitivity pneumonitis
mast cell
Journal
Immunity, inflammation and disease
ISSN: 2050-4527
Titre abrégé: Immun Inflamm Dis
Pays: England
ID NLM: 101635460
Informations de publication
Date de publication:
12 2020
12 2020
Historique:
received:
19
08
2020
accepted:
21
09
2020
pubmed:
6
10
2020
medline:
25
9
2021
entrez:
5
10
2020
Statut:
ppublish
Résumé
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. 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-β1-induced epithelial-mesenchymal transition of A549 cells was examined. 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-β1-induced epithelial-mesenchymal transition, although this trend was not observed in the chymase-treated apoA-I. 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.
Sections du résumé
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-β1-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-β1-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.
Identifiants
pubmed: 33016012
doi: 10.1002/iid3.355
pmc: PMC7654418
doi:
Substances chimiques
Apolipoprotein A-I
0
Chymases
EC 3.4.21.39
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
659-671Informations de copyright
© 2020 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.
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Immun Inflamm Dis. 2020 Dec;8(4):659-671
pubmed: 33016012