Inhibition of CtBP-regulated proinflammatory gene transcription attenuates psoriatic skin inflammation

Author(s):  
Hong Li ◽  
Caiguo Zhang ◽  
Li Bian ◽  
Hui Deng ◽  
Melanie Blevins ◽  
...  
2020 ◽  
Vol 140 (7) ◽  
pp. S83
Author(s):  
H. Li ◽  
C. Zhang ◽  
B. Li ◽  
M. Fujita ◽  
D. Norris ◽  
...  

2020 ◽  
Vol 85 ◽  
pp. 106692
Author(s):  
Quan-you Zheng ◽  
Shen-ju Liang ◽  
Feng Xu ◽  
Yi Yang ◽  
Jian-li Feng ◽  
...  

2020 ◽  
Vol 41 ◽  
pp. 101047
Author(s):  
Elizabeth A. Evans ◽  
Sophie R. Sayers ◽  
Xenia Kodji ◽  
Yue Xia ◽  
Mahum Shaikh ◽  
...  

2020 ◽  
Vol 117 (28) ◽  
pp. 16465-16474 ◽  
Author(s):  
Charlotte Hurabielle ◽  
Verena M. Link ◽  
Nicolas Bouladoux ◽  
Seong-Ji Han ◽  
Eric Dean Merrill ◽  
...  

Under steady-state conditions, the immune system is poised to sense and respond to the microbiota. As such, immunity to the microbiota, including T cell responses, is expected to precede any inflammatory trigger. How this pool of preformed microbiota-specific T cells contributes to tissue pathologies remains unclear. Here, using an experimental model of psoriasis, we show that recall responses to commensal skin fungi can significantly aggravate tissue inflammation. Enhanced pathology caused by fungi preexposure depends on Th17 responses and neutrophil extracellular traps and recapitulates features of the transcriptional landscape of human lesional psoriatic skin. Together, our results propose that recall responses directed to skin fungi can directly promote skin inflammation and that exploration of tissue inflammation should be assessed in the context of recall responses to the microbiota.


2019 ◽  
Vol 198 (3) ◽  
pp. 403-415 ◽  
Author(s):  
C. Liu ◽  
H. Liu ◽  
C. Lu ◽  
J. Deng ◽  
Y. Yan ◽  
...  

Theranostics ◽  
2020 ◽  
Vol 10 (23) ◽  
pp. 10466-10482
Author(s):  
Yuchao Chen ◽  
Yuhong Yan ◽  
Huazhen Liu ◽  
Feifei Qiu ◽  
Chun-Ling Liang ◽  
...  

Cytokine ◽  
2007 ◽  
Vol 39 (1) ◽  
pp. 28-29
Author(s):  
F. Morel ◽  
K. Boniface ◽  
E. Guignouard ◽  
N. Pedretti ◽  
M. Garcia ◽  
...  

2020 ◽  
Author(s):  
Greg A. Timblin ◽  
Kevin M. Tharp ◽  
Breanna Ford ◽  
Janet M. Winchenster ◽  
Jerome Wang ◽  
...  

AbstractMacrophages generate mitochondrial reactive oxygen and electrophilic species (mtROS, mtRES) as antimicrobials during Toll-like receptor (TLR)-dependent inflammatory responses. Whether mitochondrial stress caused by these molecules impacts macrophage function is unknown. Here we demonstrate that both pharmacologically- and lipopolysaccharide (LPS)-driven mitochondrial stress in macrophages triggers a stress response called mitohormesis. LPS-driven mitohormetic stress adaptations occur as macrophages transition from an LPS-responsive to LPS-tolerant state where stimulus-induced proinflammatory gene transcription is impaired, suggesting tolerance is a product of mitohormesis. Indeed, like LPS, pharmacologically-triggered mitohormesis suppresses mitochondrial oxidative metabolism and acetyl-CoA production needed for histone acetylation and proinflammatory gene transcription, and is sufficient to enforce an LPS-tolerant state. Thus, mtROS and mtRES are TLR-dependent signaling molecules that trigger mitohormesis as a negative feedback mechanism to restrain inflammation via tolerance. Moreover, bypassing TLR signaling and pharmacologically triggering mitohormesis represents a novel anti-inflammatory strategy that co-opts this stress response to impair epigenetic support of proinflammatory gene transcription by mitochondria.Abstract Figure


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