scholarly journals T Helper 17/Regulatory T Cell Balance and Experimental Models of Peritoneal Dialysis-Induced Damage

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Georgios Liappas ◽  
Guadalupe Tirma Gónzalez-Mateo ◽  
Pedro Majano ◽  
José Antonio Sánchez- Tomero ◽  
Marta Ruiz-Ortega ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Experimental Models ◽  
T Helper ◽  
Peritoneal Fibrosis ◽  
T Helper 17 ◽  
Th17 Response ◽  
Mesenchymal Transition ◽  
Future Goals ◽  
Clinical Biomarkers ◽  
Cell Balance

Fibrosis is a general complication in many diseases. It is the main complication during peritoneal dialysis (PD) treatment, a therapy for renal failure disease. Local inflammation and mesothelial to mesenchymal transition (MMT) are well known key phenomena in peritoneal damage during PD. New data suggest that, in the peritoneal cavity, inflammatory changes may be regulated at least in part by a delicate balance between T helper 17 and regulatory T cells. This paper briefly reviews the implication of the Th17/Treg-axis in fibrotic diseases. Moreover, it compares current evidences described in PD animal experimental models, indicating a loss of Th17/Treg balance (Th17 predominance) leading to peritoneal damage during PD. In addition, considering the new clinical and animal experimental data, new therapeutic strategies to reduce the Th17 response and increase the regulatory T response are proposed. Thus, future goals should be to develop new clinical biomarkers to reverse this immune misbalance and reduce peritoneal fibrosis in PD.

scholarly journals Corrigendum to “T Helper 17/Regulatory T Cell Balance and Experimental Models of Peritoneal Dialysis-Induced Damage”

2017 ◽  
Vol 2017 ◽  
pp. 1-1
Author(s):  
Georgios Liappas ◽  
Guadalupe Tirma Gónzalez-Mateo ◽  
Pedro Majano ◽  
José Antonio Sánchez-Tomero ◽  
Marta Ruiz-Ortega ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
T Cell ◽  
Regulatory T Cell ◽  
Experimental Models ◽  
T Helper ◽  
T Helper 17 ◽  
Cell Balance

scholarly journals FP549EARLY LEUKOCYTE ACTIVATION ANTIGEN CD69 LIMITS PERITONEAL FIBROSIS BY REGULATING THE T HELPER 17/REGULATORY T CELL BALANCE

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii257-iii257
Author(s):  
Georgios Liappas ◽  
Guadalupe Tirma González-Mateo ◽  
Rackel Díaz Sánchez ◽  
Adela Matesanz Martín ◽  
Rafal Zur ◽  
...  
Keyword(s):  
T Cell ◽  
Regulatory T Cell ◽  
Leukocyte Activation ◽  
T Helper ◽  
Peritoneal Fibrosis ◽  
T Helper 17 ◽  
Cell Balance ◽  
Activation Antigen

Glucose Degradation Products and the Peritoneal Mesothelium

2000 ◽  
Vol 20 (5_suppl) ◽  
pp. 19-22 ◽  
Author(s):  
Achim Jörres ◽  
Thorsten O. Bender ◽  
Janusz Witowski
Keyword(s):  
Peritoneal Dialysis ◽  
Degradation Products ◽  
Experimental Models ◽  
Buffer System ◽  
Peritoneal Fibrosis ◽  
High Concentration ◽  
Peritoneal Mesothelial Cells ◽  
Cell Functions ◽  
Glucose Degradation Products

Conventional heat-sterilized, glucose-based peritoneal dialysis (PD) fluids contain significant amounts of glucose degradation products (GDPs) such as aldehydes and dicarbonyl compounds (glyoxal, methylglyoxal). These GDPs have been shown to impair cell functions in various in vitro experimental models. In peritoneal mesothelial cells, GDPs dose-dependently inhibit cell proliferation and mediator synthesis. In addition, some GDPs potently promote generation of advanced glycation end-products (AGEs). Immunohistochemistry finds AGEs in the peritoneal membrane of chronic continuous ambulatory peritoneal dialysis (CAPD) patients, suggesting that peritoneal AGE accumulation may be involved in chronic peritoneal fibrosis. The formation of GDPs might be prevented by filter-sterilization of PD fluids. Another option is to separate the glucose and the buffer system in dual-chambered or multi-chambered containers. In these systems, the glucose is kept in a separate compartment at high concentration and very low pH—both conditions being known to minimize the degree of glucose decomposition during autoclaving. Initial experimental evidence suggests that these novel, multi-chambered fluids significantly improve in vitro biocompatibility; however, the clinical relevance of these results remains to be established in clinical trials.

Restoring T-helper 17 cell/regulatory T-cell balance and decreasing disease activity by rapamycin and all-trans retinoic acid in patients with systemic lupus erythematosus

Lupus ◽  
2019 ◽  
Vol 28 (12) ◽  
pp. 1397-1406 ◽  
Author(s):  
Y Chu ◽  
C Zhao ◽  
B Zhang ◽  
X Wang ◽  
Y Wang ◽  
...  
Keyword(s):  
Disease Activity ◽  
Lupus Erythematosus ◽  
Treg Cells ◽  
T Helper ◽  
T Helper 17 ◽  
Sledai Score ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Before And After ◽  
Cell Balance

Objective This study aimed to investigate the effect of rapamycin (RAPA) alone or in combination with all-trans retinoic acid (ATRA) on the T-helper 17 (Th17) cell/regulatory T-cell (Treg) balance in patients with systemic lupus erythematosus (SLE) and to evaluate the clinical efficacy. Methods Seventy patients with SLE were enrolled. They were randomly and equally divided into RAPA and RAPA + ATRA groups. The number of Th17 and Treg cells was measured by flow cytometry before and after treatment for 6, 12 and 24 weeks. The SLE Disease Activity Index (SLEDAI) score and the prednisone dose before and after treatment were used to evaluate the efficacy between the two groups. Results In both groups, at different time points after treatment, the number of Th17 cells ( p = 0.003) and Th17/Treg ratio ( p = 0.044) reduced, while the number of Treg cells ( p = 0.574) tended to increase. The SLEDAI score and the dose of prednisone decreased significantly ( p < 0.001). There was no significant difference in the number of Th17 cells ( p = 0.089), Treg cells ( p = 0.059), Th17/Treg ratio ( p = 0.580), SLEDAI score ( p = 0.127) and the dose of prednisone ( p = 0.329) between the two groups. Conclusion Disease activity in SLE patients reduced with RAPA alone or in conjunction with ATRA, reducing glucocorticoid requirement. One of its mechanisms of action may be regulating the Th17/Treg cell balance, which provides a new model for the pathogenesis and potential treatment of SLE.

scholarly journals Nitro-oleic acid inhibits the high glucose-induced epithelial-mesenchymal transition in peritoneal mesothelial cells and attenuates peritoneal fibrosis

2020 ◽  
Vol 318 (2) ◽  
pp. F457-F467
Author(s):  
Wenyan Su ◽  
Haiping Wang ◽  
ZiYan Feng ◽  
Jing Sun
Keyword(s):  
Peritoneal Dialysis ◽  
Oleic Acid ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Smooth Muscle Actin ◽  
Transforming Growth Factor Β ◽  
Muscle Actin ◽  
Peritoneal Fibrosis ◽  
Mesenchymal Transition ◽  
Peritoneal Mesothelial Cells

As an electrophilic nitroalkene fatty acid, nitro-oleic acid (OA-NO2) exerts multiple biological effects that contribute to anti-inflammation, anti-oxidative stress, and antiapoptosis. However, little is known about the role of OA-NO2 in peritoneal fibrosis. Thus, in the present study, we examined the effects of OA-NO2 on the high glucose (HG)-induced epithelial-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs) and evaluated the morphological and immunohistochemical changes in a rat model of peritoneal dialysis-related peritoneal fibrosis. In in vitro experiments, we found that HG reduced the expression level of E-cadherin and increased Snail, N-cadherin, and α-smooth muscle actin expression levels in HPMCs. The above-mentioned changes were attenuated by pretreatment with OA-NO2. Additionally, OA-NO2 also inhibited HG-induced activation of the transforming growth factor-β1/Smad signaling pathway and NF-κB signaling pathway. Meanwhile, OA-NO2 inhibited HG-induced phosphorylation of Erk and JNK. The results from the in vivo experiments showed that OA-NO2 notably relieved peritoneal fibrosis by decreasing the thickness of the peritoneum; it also inhibited expression of transforming growth factor-β1, α-smooth muscle actin, N-cadherin, and vimentin and enhanced expression of E-cadherin in the peritoneum. Collectively, these results suggest that OA-NO2 inhibits the HG-induced epithelial-mesenchymal transition in HPMCs and attenuates peritoneal dialysis-related peritoneal fibrosis.

scholarly journals Effect of Milk Fermented with Lactobacillus fermentum on the Inflammatory Response in Mice

Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1039 ◽  
Author(s):  
Lourdes Santiago-López ◽  
Adrián Hernández-Mendoza ◽  
Verónica Mata-Haro ◽  
Belinda Vallejo-Córdoba ◽  
Abraham Wall-Medrano ◽  
...  
Keyword(s):  
Fermented Milk ◽  
Lactobacillus Fermentum ◽  
Spleen Weight ◽  
T Helper ◽  
Bacterial Concentration ◽  
T Helper 17 ◽  
Th17 Response ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Infusion Protocol

Currently, the effect of fermented milk on the T-helper 17 response in inflammatory bowel diseases (IBDs) is unknown. The aim of the present study was to evaluate the effect of milks fermented with Lactobacillus fermentum on the Th1/Th17 response in a murine model of mild IBD. Exopolysaccharide (EPS), lactic acid (LA), and total protein (TP) contents and bacterial concentration were determined. Male C57Bl/6 mice intragastrically received either raw (FM) or pasteurized (PFM) fermented milk before and during a dextran sulfate infusion protocol. Blood, spleen, and colon samples were collected at Weeks 6 and 10. IL-6, IL-10, and TNFα were determined in serum, and IL-17, IL-23, and IFNγ were determined in intestinal mucosa and serum. The FM groups did not differ in cell concentration, LA, or TP content (p > 0.05); FM-J28 had the highest EPS content. Spleen weight and colon length did not differ among the FM groups (p > 0.05). In the FM-J20 and PFM-J20 groups, IL-17 and IFNγ decreased, and the IL-10 concentration was enhanced (p < 0.05) at Week 6. IL-6, TNFα, IL-23, and IFNγ did not differ in serum and mucosa (p > 0.05), and IL-17 was lowest in FM-J28 and FM-J20. Therefore, FM appears to potentially play a role in decreasing the Th17 response. However, further studies are needed to elucidate the FM-mediated anti-inflammatory mechanisms in IBD.

scholarly journals Dipeptidyl peptidase 4 promotes peritoneal fibrosis and its inhibitions prevent failure of peritoneal dialysis

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yi-Chen Li ◽  
Pei-Hsun Sung ◽  
Yao-Hsu Yang ◽  
John Y. Chiang ◽  
Hon-Kan Yip ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Epithelial Mesenchymal Transition ◽  
Dipeptidyl Peptidase ◽  
Diabetic Patients ◽  
Peritoneal Fibrosis ◽  
High Concentration ◽  
Mesenchymal Transition ◽  
Dipeptidyl Peptidase 4 ◽  
Stage Renal Disease ◽  
End Stage

AbstractPeritoneal dialysis (PD) possesses multiple advantages for end stage renal disease. However, long-term PD triggers peritoneal fibrosis (PF). From the nationwide analysis of diabetic PD patients (n = 19,828), we identified the incidence of PD failure was significantly lower in diabetic patients treated with dipeptidyl peptidase 4 (DPP4) inhibitors. Experimental study further showed high concentration of glucose remarkably enhanced DPP4 to promote epithelial-mesenchymal transition (EMT) in the mesothelial cells. In chlorhexidine gluconate (CG)-induced PF model of rats, DPP4 expression was enriched at thickening peritoneum. Moreover, as to CG-induced PF model, DPP4 deficiency (F344/DuCrlCrlj strain), sitagliptin and exendin-4 treatments significantly inhibited DPP4 to reverse the EMT process, angiogenesis, oxidative stress, and inflammation, resulting in the protection from PF, preservation of peritoneum and the corresponding functional integrity. Furthermore, DPP4 activity was significantly correlated with peritoneal dysfunction. Taken together, DPP4 caused peritoneal dysfunction/PF, whereas inhibition of DPP4 protected the PD patients against PD failure.

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