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2017 ; 7
(1
): 9235
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Mitigation of sepsis-induced inflammatory responses and organ injury through
targeting Wnt/?-catenin signaling
#MMPMID28835626
Sharma A
; Yang WL
; Ochani M
; Wang P
Sci Rep
2017[Aug]; 7
(1
): 9235
PMID28835626
show ga
The Wnt/?-catenin pathway has been involved in regulating inflammation in various
infectious and inflammatory diseases. Sepsis is a life-threatening condition
caused by dysregulated inflammatory response to infection with no effective
therapy available. Recently elevated Wnt/?-catenin signaling has been detected in
sepsis. However, its contribution to sepsis-associated inflammatory response
remains to be explored. In this study, we show that inhibition of Wnt/?-catenin
signaling reduces inflammation and mitigates sepsis-induced organ injury. Using
in vitro LPS-stimulated RAW264.7 macrophages, we demonstrate that a
small-molecule inhibitor of ?-catenin responsive transcription, iCRT3,
significantly reduces the LPS-induced Wnt/?-catenin activity and also inhibits
TNF-? production and I?B degradation in a dose-dependent manner. Intraperitoneal
administration of iCRT3 to C57BL/6 mice, subjected to cecal ligation and
puncture-induced sepsis, decreases the plasma levels of proinflammatory cytokines
and organ injury markers in a dose-dependent manner. The histological integrity
of the lungs is improved with iCRT3 treatment, along with reduced lung collagen
deposition and apoptosis. In addition, iCRT3 treatment also decreases the
expression of the cytokines, neutrophil chemoattractants, as well as the MPO
activity in the lungs of septic mice. Based on these findings we conclude that
targeting the Wnt/?-Catenin pathway may provide a potential therapeutic approach
for treatment of sepsis.
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