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2016 ; 71
(6
): 565-7
Nephropedia Template TP
gab.com Text
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English Wikipedia
Caffeine inhibits TGF? activation in epithelial cells, interrupts fibroblast
responses to TGF?, and reduces established fibrosis in ex vivo precision-cut lung
slices
#MMPMID26911575
Tatler AL
; Barnes J
; Habgood A
; Goodwin A
; McAnulty RJ
; Jenkins G
Thorax
2016[Jun]; 71
(6
): 565-7
PMID26911575
show ga
Caffeine is a commonly used food additive found naturally in many products. In
addition to potently stimulating the central nervous system caffeine is able to
affect various systems within the body including the cardiovascular and
respiratory systems. Importantly, caffeine is used clinically to treat apnoea and
bronchopulmonary dysplasia in premature babies. Recently, caffeine has been shown
to exhibit antifibrotic effects in the liver in part through reducing collagen
expression and deposition, and reducing expression of the profibrotic cytokine
TGF?. The potential antifibrotic effects of caffeine in the lung have not
previously been investigated. Using a combined in vitro and ex vivo approach we
have demonstrated that caffeine can act as an antifibrotic agent in the lung by
acting on two distinct cell types, namely epithelial cells and fibroblasts.
Caffeine inhibited TGF? activation by lung epithelial cells in a
concentration-dependent manner but had no effect on TGF? activation in
fibroblasts. Importantly, however, caffeine abrogated profibrotic responses to
TGF? in lung fibroblasts. It inhibited basal expression of the ?-smooth muscle
actin gene and reduced TGF?-induced increases in profibrotic genes. Finally,
caffeine reduced established bleomycin-induced fibrosis after 5?days treatment in
an ex vivo precision-cut lung slice model. Together, these findings suggest that
there is merit in further investigating the potential use of caffeine, or its
analogues, as antifibrotic agents in the lung.