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2018 ; 2018
(ä): 7934362
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TRAIL-Dependent Resolution of Pulmonary Fibrosis
#MMPMID29670467
Habiel DM
; Moreira AP
; Ismailoglu UB
; Dunleavy MP
; Cavassani KA
; van Rooijen N
; Coelho AL
; Hogaboam CM
Mediators Inflamm
2018[]; 2018
(ä): 7934362
PMID29670467
show ga
Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung
disease characterized by the persistence of activated myofibroblasts resulting in
excessive deposition of extracellular matrix proteins and profound tissue
remodeling. In the present study, the expression of tumor necrosis factor- (TNF-)
related apoptosis-inducing ligand (TRAIL) was key to the resolution of
bleomycin-induced pulmonary fibrosis. Both in vivo and in vitro studies
demonstrated that Gr-1(+)TRAIL(+) bone marrow-derived myeloid cells blocked the
activation of lung myofibroblasts. Although soluble TRAIL was increased in plasma
from IPF patients, the presence of TRAIL(+) myeloid cells was markedly reduced in
IPF lung biopsies, and primary lung fibroblasts from this patient group expressed
little of the TRAIL receptor-2 (DR5) when compared with appropriate normal
samples. IL-13 was a potent inhibitor of DR5 expression in normal fibroblasts.
Together, these results identified TRAIL(+) myeloid cells as a critical mechanism
in the resolution of pulmonary fibrosis, and strategies directed at promoting its
function might have therapeutic potential in IPF.
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