scholarly journals Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the STAT3 Signaling Pathway and Regulation of the between Th17/Treg Balance

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0135858 ◽  
Author(s):  
Seon-Yeong Lee ◽  
Seung Hoon Lee ◽  
Eun-Ji Yang ◽  
Eun-Kyung Kim ◽  
Jae-Kyung Kim ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Signaling Pathway ◽  
Bowel Disease ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Inflammatory Bowel

Lactobacillus paracasei L9 improves colitis by expanding butyrate-producing bacteria that inhibits the IL-6/STAT3 signaling pathway

2021 ◽  
Author(s):  
Zhengquan Yu ◽  
Min Deng ◽  
Xi Wu ◽  
Xiaoyue Duan ◽  
Jiuzhi Xu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Signaling Pathway ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Lactobacillus Paracasei ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

Inflammatory bowel disease (IBD) is a chronic intestinal inflammation that is currently incurable. Increasing evidences indicate that supplementation with probiotics could improve the symptoms of IBD. It is scientifically significant...

Very early onset inflammatory bowel disease: Investigation of the IL-10 signaling pathway in Iranian children

2017 ◽  
Vol 60 (12) ◽  
pp. 643-649 ◽  
Author(s):  
Shahram Nemati ◽  
Shahram Teimourian ◽  
Mina Tabrizi ◽  
Mehri Najafi ◽  
Naghi Dara ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Signaling Pathway ◽  
Bowel Disease ◽  
Early Onset ◽  
Inflammatory Bowel ◽  
Iranian Children

scholarly journals Noncanonical NF-κB Signaling Upregulation in Inflammatory Bowel Disease Patients is Associated With Loss of Response to Anti-TNF Agents

2021 ◽  
Vol 12 ◽  
Author(s):  
Vu Q. Nguyen ◽  
Kristin Eden ◽  
Holly A. Morrison ◽  
Megan B. Sammons ◽  
Kristin K. Knight ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Signaling Pathway ◽  
Bowel Disease ◽  
Target Genes ◽  
Preliminary Evidence ◽  
Lymphocyte Migration ◽  
Clinical Criteria ◽  
Number Of Patients ◽  
Effective Therapeutic Strategy ◽  
Inflammatory Bowel

Objectives: Targeting tumor necrosis factor (TNF) with biologic agents, such as infliximab and adalimumab, is a widely used and effective therapeutic strategy in inflammatory bowel disease (IBD). Unfortunately, a significant number of patients fail to respond or lose response over time to these agents. Previous studies have defined multiple complex roles for canonical NF-κB signaling in the pathogenesis of IBD. However, preliminary evidence suggests that the lesser defined noncanonical NF-κB signaling pathway also contributes to disease pathogenesis and response to anti-TNF agents. The objective of this study was to evaluate this hypothesis in Crohn’s disease (CD) and ulcerative colitis (UC) patients.Design: A total of 27 subjects with IBD (19 with CD and 8 with UC) and 15 control subjects were tested. Clinical criteria, patient history, and endoscopic disease activity were factors used to categorize patients and define therapeutic response. Biopsy specimens were collected during colonoscopy and expression was determined for 88 target genes known to be associated with noncanonical NF-κB signaling and IBD.Results: Noncanonical NF-κB signaling was significantly upregulated in IBD patients and was associated with increased gastrointestinal inflammation, epithelial cell death, lymphocyte migration, and Nod-like receptor signaling. Furthermore, noncanonical NF-κB signaling was further upregulated in patients unresponsive to anti-TNF agents and was suppressed in responsive patients. MAP3K14, NFKB2, CCL19, CXCL12, and CXCL13 were significantly dysregulated, as were genes that encode pathway regulators, such as CYLD, NLRP12, and BIRC2/3.Conclusion: Our study identifies a previously uncharacterized role for the understudied noncanonical NF-κB signaling pathway in the pathogenesis of IBD and anti-TNF therapy responsiveness. The genes and pathways identified may ultimately prove useful in IBD management and could potentially be used as biomarkers of drug response.

557 Epigenetic Regulation of WNT Signaling Pathway Genes in Inflammatory Bowel Disease (IBD) Neoplasia

2008 ◽  
Vol 134 (4) ◽  
pp. A-848-A-849
Author(s):  
Mashaal Dhir ◽  
Elizabeth A. Montgomery ◽  
Kornel Schuebel ◽  
Susan L. Gearhart ◽  
Nita Ahuja
Keyword(s):  
Inflammatory Bowel Disease ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Epigenetic Regulation ◽  
Bowel Disease ◽  
Wnt Signaling Pathway ◽  
Inflammatory Bowel

scholarly journals Deleterious Genetic Variation Across the NOD Signaling Pathway Is Associated With Reduced NFKB Signaling Transcription and Upregulation of Alternative Inflammatory Transcripts in Pediatric Inflammatory Bowel Disease

2022 ◽  
Author(s):  
James J Ashton ◽  
Konstantinos Boukas ◽  
Imogen S Stafford ◽  
Guo Cheng ◽  
Rachel Haggarty ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Signaling Pathway ◽  
Bowel Disease ◽  
Intestinal Bacteria ◽  
Genomic Variation ◽  
Gene Score ◽  
Diagnostic Endoscopy ◽  
Pediatric Inflammatory Bowel Disease ◽  
Inflammatory Bowel ◽  
The Impact

Abstract Background Inflammatory bowel disease may arise with inadequate immune response to intestinal bacteria. NOD2 is an established gene in Crohn’s disease pathogenesis, with deleterious variation associated with reduced NFKB signaling. We hypothesized that deleterious variation across the NOD2 signaling pathway impacts on transcription. Methods Treatment-naïve pediatric inflammatory bowel disease patients had ileal biopsies for targeted autoimmune RNA-sequencing and blood for whole exome sequencing collected at diagnostic endoscopy. Utilizing GenePy, a per-individual, per-gene score, genes within the NOD signaling pathway were assigned a quantitative score representing total variant burden. Where multiple genes formed complexes, GenePy scores were summed to create a “complex” score. Normalized transcript expression of 95 genes within this pathway was retrieved. Regression analysis was performed to determine the impact of genomic variation on gene transcription. Results Thirty-nine patients were included. Limited clustering of patients based on NOD signaling transcripts was related to underlying genomic variation. Patients harboring deleterious variation in NOD2 had reduced NOD2 (β = -0.702, P = 4.3 × 10-5) and increased NFKBIA (β = 0.486, P = .001), reflecting reduced NFKB signal activation. Deleterious variation in the NOD2-RIPK2 complex was associated with increased NLRP3 (β = 0.8, P = 3.1475 × 10-8) and TXN (β = -0.417, P = 8.4 × 10-5) transcription, components of the NLRP3 inflammasome. Deleterious variation in the TAK1-TAB complex resulted in reduced MAPK14 transcription (β = -0.677, P = 1.7 × 10-5), a key signal transduction protein in the NOD2 signaling cascade and increased IFNA1 (β = 0.479, P = .001), indicating reduced transcription of NFKB activators and alternative interferon transcription in these patients. Conclusions Data integration identified perturbation of NOD2 signaling transcription correlated with genomic variation. A hypoimmune NFKB signaling transcription response was observed. Alternative inflammatory pathways were activated and may represent therapeutic targets in specific patients.

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