Integrative analysis of transcriptome‐wide association study data and messenger RNA expression profiles identified candidate genes and pathways for inflammatory bowel disease

2019 ◽  
Vol 120 (9) ◽  
pp. 14831-14837 ◽  
Author(s):  
Bolun Cheng ◽  
Xiao Liang ◽  
Yan Wen ◽  
Ping Li ◽  
Lu Zhang ◽  
...  
2013 ◽  
Vol 173 (2) ◽  
pp. 250-258 ◽  
Author(s):  
M. Iborra ◽  
F. Bernuzzi ◽  
C. Correale ◽  
S. Vetrano ◽  
G. Fiorino ◽  
...  

2013 ◽  
Vol 7 ◽  
pp. S284
Author(s):  
M. Iborra ◽  
F. Bernuzzi ◽  
B. Beltrán ◽  
M. Locati ◽  
P. Nos ◽  
...  

2014 ◽  
Vol 20 (5) ◽  
pp. 777-782 ◽  
Author(s):  
Karin Fransen ◽  
Suzanne van Sommeren ◽  
Harm-Jan Westra ◽  
Monique Veenstra ◽  
Letitia E. Lamberts ◽  
...  

2011 ◽  
Vol 140 (5) ◽  
pp. S-273
Author(s):  
Marisa Iborra ◽  
Francesca Bernuzzi ◽  
Belen Beltran ◽  
Antonino Spinelli ◽  
Pietro Invernizzi ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Juan Du ◽  
Jie Yin ◽  
Haojie Du ◽  
Jiawei Zhang

The aim of this study was to investigate the expression features of discordant inflammatory bowel disease (IBD) twin pairs to identify novel molecular features and markers. We collected an expression dataset of discordant twin pairs with ulcerative colitis and performed integrative analysis to identify the genetic-independent expression features. Through deconvolution of the immune cell populations and tissue expression specificity, we refined the candidate genes for susceptibility to ulcerative colitis. We found that dysregulated immune systems and NOD-related pathways were enriched in the expression network of the discordant IBD twin pairs. Among the identified factors were significantly increased proportions of immune cells, including megakaryocytes, neutrophils, natural killer T cells, and lymphatic endothelial cells. The differentially expressed genes were significantly enriched in a gene set associated with cortical and medullary thymocytes. Finally, by combining these expression features with genetic resources, we identified some candidate genes with potential to serve as novel markers of ulcerative colitis, such as CYP2C18. Ulcerative colitis is a subtype of inflammatory bowel disease and a polygenic disorder. Through integrative analysis, we identified some genes, such as CYP2C18, that are involved in the pathogenesis of IBD as well as some candidate therapeutic targets, such as LOXL2.


Author(s):  
Daniele Piovani ◽  
Claudia Pansieri ◽  
Soumya R R Kotha ◽  
Amanda C Piazza ◽  
Celia-Louise Comberg ◽  
...  

Abstract Background and aims The association between smoking and inflammatory bowel disease (IBD) relies on old meta-analyses including exclusively non-Jewish White populations. Uncertainty persists regarding the role of smoking in other ethnicities. Methods We systematically searched Medline/PubMed, Embase and Scopus for studies examining tobacco smoking and the risk of developing IBD, i.e., Crohn’s disease (CD) or ulcerative colitis (UC). Two authors independently extracted study data and assessed each study’s risk-of-bias. We examined heterogeneity and small-study effect, and calculated summary estimates using random-effects models. Stratified analyses and meta-regression were employed to study the association between study-level characteristics and effect estimates. The strength of epidemiological evidence was assessed through prespecified criteria. Results We synthesized 57 studies examining the smoking-related risk of developing CD and UC. Non-Jewish White smokers were at increased risk of CD (29 studies; RR: 1.95, 95% CI: 1.69‒2.24; moderate evidence). No association was observed in Asian, Jewish and Latin-American populations (11 studies; RR: 0.97; 95% CI: 0.83–1.13), with no evidence of heterogeneity across these ethnicities. Smokers were at reduced risk of UC (51 studies; RR: 0.55, 95% CI: 0.48–0.64; weak evidence) irrespectively of ethnicity; however, cohort studies, large studies and those recently published showed attenuated associations. Conclusions This meta-analysis did not identify any increased risk of CD in smokers in ethnicities other than non-Jewish Whites, and confirmed the protective effect of smoking on UC occurrence. Future research should characterize the genetic background of CD patients across different ethnicities to improve our understanding on the role of smoking in CD pathogenesis.


Sign in / Sign up

Export Citation Format

Share Document