P332 Role of toll-like receptor signaling in epithelial barrier dysfunction in eosinophilic esophagitis

2017 ◽  
Vol 119 (5) ◽  
pp. S78-S79
Author(s):  
M. Ruffner ◽  
S. Raman ◽  
K. Mauer ◽  
A. Muir ◽  
J. Spergel ◽  
...  
Keyword(s):  
Eosinophilic Esophagitis ◽  
Epithelial Barrier ◽  
Receptor Signaling ◽  
Toll Like Receptor ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Dysfunction

scholarly journals The role of secreted Hsp90α in HDM-induced asthmatic airway epithelial barrier dysfunction

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Cuiping Ye ◽  
Chaowen Huang ◽  
Mengchen Zou ◽  
Yahui Hu ◽  
Lishan Luo ◽  
...  
Keyword(s):  
Barrier Function ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Function ◽  
Asthmatic Airway ◽  
Epithelial Barrier Dysfunction

Abstract Background The dysfunction of airway epithelial barrier is closely related to the pathogenesis of asthma. Secreted Hsp90α participates in inflammation and Hsp90 inhibitor protects endothelial dysfunction. In the current study, we aimed to explore the role of secreted Hsp90α in asthmatic airway epithelial barrier function. Methods Male BALB/c mice were sensitized and challenged with HDM to generate asthma model. The 16HBE and Hsp90α-knockdown cells were cultured and treated according to the experiment requirements. Transepithelial Electric Resistance (TEER) and permeability of epithelial layer in vitro, distribution and expression of junction proteins both in vivo and in vitro were used to evaluate the epithelial barrier function. Western Blot was used to evaluate the expression of junction proteins and phosphorylated AKT in cells and lung tissues while ELISA were used to evaluate the Hsp90α expression and cytokines release in the lung homogenate. Results HDM resulted in a dysfunction of airway epithelial barrier both in vivo and in vitro, paralleled with the increased expression and release of Hsp90α. All of which were rescued in Hsp90α-knockdown cells or co-administration of 1G6-D7. Furthermore, either 1G6-D7 or PI3K inhibitor LY294002 suppressed the significant phosphorylation of AKT, which caused by secreted and recombinant Hsp90α, resulting in the restoration of epithelial barrier function. Conclusions Secreted Hsp90α medicates HDM-induced asthmatic airway epithelial barrier dysfunction via PI3K/AKT pathway, indicating that anti-secreted Hsp90α therapy might be a potential treatment to asthma in future.

201 Claudin-7 Dysregulation in Pediatric Eosinophilic Esophagitis: A Role for TGF-β in Esophageal Epithelial Barrier Dysfunction

2015 ◽  
Vol 148 (4) ◽  
pp. S-51
Author(s):  
Shahan D. Fernando ◽  
Kathryn A. Biette ◽  
Glenn Furuta ◽  
Joanne C. Masterson
Keyword(s):  
Eosinophilic Esophagitis ◽  
Epithelial Barrier ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Dysfunction

scholarly journals Inactivation of the Wnt/β-catenin signaling contributes to the epithelial barrier dysfunction induced by sodium oxalate in canine renal epithelial cells

2021 ◽  
Author(s):  
Yun Ji ◽  
Shuting Fang ◽  
Ying Yang ◽  
Zhenlong Wu
Keyword(s):  
Epithelial Cells ◽  
Barrier Function ◽  
Mdck Cells ◽  
Renal Stones ◽  
Sodium Oxalate ◽  
Epithelial Barrier ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Function ◽  
Epithelial Barrier Dysfunction

Abstract Background Nephrolithiasis (also known as renal stones) is a common disease condition in companion animals, including dogs and cats. Dysfunction of renal tubular epithelial cells involves in the pathogenesis of renal stones. However, a functional role of Wnt/β-catenin signaling and its contribution to nephrolithiasis remains unknown. Results In the present study, we found that Mardin-Darby canine kidney (MDCK) cells treated with sodium oxalate resulted in reduced cell proliferation and migration, which was associated with the G0/G1 phase arrest of cell cycle progression. In addition, sodium oxalate exposure led to decreased transepithelial electrical resistance (TEER) and increased paracellular permeability. The deleterious effect of sodium oxalate on epithelial barrier function was related to decreased protein abundances of claudin-1, occludin, zonula occludens (ZO)-1, ZO-2 and ZO-3. Of note, protein levels of p-β-catenin (Ser552) in MDCK cells were repressed by sodium oxalate, indicating an inhibitory effect on the Wnt/β-catenin signaling. Intriguingly, SB216763, a GSK-3β inhibitor, enhanced the expression p-β-catenin (Ser552), and protected against epithelial barrier dysfunction in sodium oxalate-treated MDCK cells. Conclusion Taken together, our results revealed a critical role of Wnt/β-catenin signaling on the epithelial barrier function of MDCK cells. Activation of Wnt/β-catenin signaling might be an potentially therapeutic target for the treatment of renal stones in animals.

Role of focal adhesion kinase in burn induced gut epithelial barrier dysfunction

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Fang Wang ◽  
Rebecca A. Eitnier ◽  
Alexandra M. Aponte ◽  
Thomas J. Ewing ◽  
Mack H. Wu
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Epithelial Barrier ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Dysfunction

Role of microRNAs in regulation of T17-driven airway epithelial barrier dysfunction

2020 ◽  
Author(s):  
Elisabeth Ax ◽  
Henric Olsson ◽  
Cecilia Lässer ◽  
Zala Jevnikar ◽  
Madeleine Rådinger
Keyword(s):  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Dysfunction

scholarly journals Protective effects of lactic acid bacteria on gut epithelial barrier dysfunction are Toll like receptor 2 and protein kinase C dependent

2020 ◽  
Vol 11 (2) ◽  
pp. 1230-1234
Author(s):  
Chengcheng Ren ◽  
Qiuxiang Zhang ◽  
Bart J. de Haan ◽  
Marijke M. Faas ◽  
Hao Zhang ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Epithelial Barrier ◽  
Protective Effects ◽  
Toll Like Receptor ◽  
Bacterial Strains ◽  
Barrier Dysfunction ◽  
Barrier Integrity ◽  
Kinase C ◽  
Toll Like Receptor 2 ◽  
Epithelial Barrier Dysfunction

TLR2-signalling lactic acid bacterial strains specifically inhibit PKC-dependent gut epithelial barrier integrity loss but cannot dampen MAPK-dependent epithelial barrier disruption.

Sign in / Sign up

Export Citation Format

Share Document