Tu1734 A Role of iRhom2 for the Secretion of TNF-α in Inflammatory Bowel Disease

AbstractRecently the role of Parkinson’s disease 7 (PARK7) was studied in gastrointestinal diseases, however, the complex role of PARK7 in the intestinal inflammation is still not completely clear. Expression and localization of PARK7 were determined in the colon biopsies of children with inflammatory bowel disease (IBD), in the colon of dextran sodium sulphate (DSS) treated mice and in HT-29 colonic epithelial cells treated with interleukin (IL)-17, hydrogen peroxide (H2O2), tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β or lipopolysaccharide (LPS). Effect of PARK7 on the synthesis of IBD related cytokines was determined using PARK7 gene silenced HT-29 cells and 3,4,5-trimethoxy-N-(4-(8-methylimidazo(1,2-a)pyridine-2-yl)phenyl)benzamide (Comp23)—compound increasing PARK7 activity—treated mice with DSS-colitis. PARK7 expression was higher in the mucosa of children with Crohn’s disease compared to that of controls. While H2O2 and IL-17 treatment increased, LPS, TNF-α or TGF-β treatment decreased the PARK7 synthesis of HT-29 cells. PARK7 gene silencing influenced the synthesis of IL1B, IL6, TNFA and TGFB1 in vitro. Comp23 treatment attenuated the ex vivo permeability of colonic sacs, the clinical symptoms, and mucosal expression of Tgfb1, Il1b, Il6 and Il10 of DSS-treated mice. Our study revealed the role of PARK7 in the regulation of IBD-related inflammation in vitro and in vivo, suggesting its importance as a future therapeutic target.

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Role of leptin and TNF-α in energy metabolism regulation in patients with inflammatory bowel disease

Digestive and Liver Disease ◽

10.1016/s1590-8658(00)80199-1 ◽

2000 ◽

Vol 32 ◽

pp. A39

Author(s):

E. Capristo ◽

G. Addolorato ◽

A. Scarfone ◽

G. Valentini ◽

G. Mingrone ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Energy Metabolism ◽

Bowel Disease ◽

Metabolism Regulation ◽

Tnf Α ◽

Inflammatory Bowel

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Cytokines in canine inflammatory bowel disease

Polish Journal of Veterinary Sciences ◽

10.2478/pjvs-2013-0025 ◽

2013 ◽

Vol 16 (1) ◽

pp. 165-171 ◽

Cited By ~ 13

Author(s):

A. Kołodziejska-Sawerska ◽

A. Rychlik ◽

A. Depta ◽

M. Wdowiak ◽

M. Nowicki ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Mrna Expression ◽

Lamina Propria ◽

Bowel Disease ◽

Unknown Etiology ◽

Tnf Α ◽

Chronic Enteropathies ◽

Inflammatory Bowel ◽

Ifn Γ

Abstract Canine inflammatory bowel disease is a group of chronic enteropathies characterized by persistent or recurring gastric symptoms with an unknown etiology which are related to histopathological changes in the mucosa of the small and large bowel in the form of cellular infiltration in the mucosal lamina propria. Recent years have witnessed a growing number of investigations into the role of the immune system and, in particular, cytokines in the development of IBD. In this article, the expression of pro-inflammatory (IL-1, IL-2, IL-5, IL-6, IL-12, IL-18, IFN-γ, TNF-α) and anti-inflammatory cytokines (IL-4, IL-10) was compared in canine patients with IBD based on clinical presentation, breed, lamina propria cell infiltrate and histopathological grade. Only selected studies confirmed higher mRNA expression levels of cytokines IL-2, IL-4, IL-5, IL-12p40, IFN-γ, TNF-α and TGF-β in dogs with IBD in comparison with healthy subjects. GSD were strongly represented in most study populations. Dogs with LPE were characterized by elevated levels of IL-1α, IL-1β, IL-2, IL-5, IL-6, IL-12, TNF-α, TGF-β. The present studies of canine patients with LPC revealed the mRNA expression of cytokines IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12p35, IL-12p40, IFN-γ, TNF-α, TGF-β. In the reviewed studies, the progression of IBD was not accompanied by changes in the mRNA expression of IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-18, TNF-α, IFN-γ or TGF-β.

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STAT1 epigenetically regulates LCP2 and TNFAIP2 by recruiting EP300 to contribute to the pathogenesis of inflammatory bowel disease

Clinical Epigenetics ◽

10.1186/s13148-021-01101-w ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Ya-Li Yu ◽

Meng Chen ◽

Hua Zhu ◽

Ming-Xing Zhuo ◽

Ping Chen ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Target Genes ◽

Dextran Sulfate ◽

Rna Seq ◽

Acute Colitis ◽

Tnf Α ◽

Inflammatory Bowel ◽

Inducible Protein

Abstract Background The aetiology of inflammatory bowel disease (IBD) is related to genetics and epigenetics. Epigenetic regulation of the pathogenesis of IBD has not been well defined. Here, we investigated the role of H3K27ac events in the pathogenesis of IBD. Based on previous ChIP-seq and RNA-seq assays, we studied signal transducer and activator of transcription 1 (STAT1) as a transcription factor (TF) and investigated whether the STAT1–EP300–H3K27ac axis contributes to the development of IBD. We performed ChIP-PCR to investigate the interaction between STAT1 and H3K27ac, and co-IP assays were performed to investigate the crosstalk between STAT1 and EP300. Results Lymphocyte cytosolic protein 2 (LCP2) and TNF-α‐inducible protein 2 (TNFAIP2) are target genes of STAT1. p-STAT1 binds to the enhancer loci of the two genes where H3K27ac is enriched, and EP300 subsequently binds to regulate their expression. In mice with dextran sulfate sodium (DSS)-induced acute colitis, an EP300 inhibitor significantly inhibited colitis. Conclusions p-STAT1 and EP300 promote TNFAIP2 and LCP2 expression through an increase in H3K27ac enrichment on their enhancers and contribute to the pathogenesis of chronic inflammation. Graphic abstract

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The role of osteopontin (OPN/SSP1) gene variants in inflammatory bowel disease

Zeitschrift für Gastroenterologie ◽

10.1055/s-0029-1241334 ◽

2009 ◽

Vol 47 (09) ◽

Author(s):

J Glas ◽

J Seiderer ◽

HP Török ◽

B Göke ◽

T Ochsenkühn ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Gene Variants ◽

Inflammatory Bowel

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Nutrition in inflammatory bowel disease

Orvosi Hetilap ◽

10.1556/oh.2009.28599 ◽

2009 ◽

Vol 150 (18) ◽

pp. 839-845 ◽

Cited By ~ 2

Author(s):

János Banai

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Fast Food ◽

Optimal Growth ◽

Developed Countries ◽

Aetiological Factor ◽

Artificial Nutrition ◽

Food Preservatives ◽

Inflammatory Bowel

Aetiology of inflammatory bowel disease (IBD) is complex and probably multifactorial. Nutrition has been proposed to be an important aetiological factor for development of IBD. Several components of the diet (such as sugar, fat, fibre, fruit and vegetable, protein, fast food, preservatives etc.) were examined as possible causative agents for IBD. According to some researchers infant feeding (breast feeding) may also contribute to the development of IBD. Though the importance of environmental factors is evidenced by the increasing incidence in developed countries and in migrant population in recent decades, the aetiology of IBD remained unclear. There are many theories, but as yet no dietary approaches have been proved to reduce the risk of developing IBD. The role of nutrition in the management of IBD is better understood. The prevention and correction of malnutrition, the provision of macro- and micronutrients and vitamins and the promotion of optimal growth and development of children are key points of nutritional therapy. In active disease, the effective support of energy and nutrients is a very important part of the therapy. Natural and artificial nutrition or the combination of two can be choosen for supporting therapy of IBD. The author summarises the aetiological and therapeutic role of nutrition in IBD.

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Role of Rifaximin in Inflammatory Bowel Disease Treatment

Mini-Reviews in Medicinal Chemistry ◽

10.2174/1389557515666150722104230 ◽

2015 ◽

Vol 16 (3) ◽

pp. 225-229 ◽

Cited By ~ 2

Author(s):

Maria Lia Scribano

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Disease Treatment ◽

Inflammatory Bowel

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Tu1789 – Treatment Response to Ustekinumab and Vedolizumab in Inflammatory Bowel Disease: the Predictive Role of Gut Microbiota

Gastroenterology ◽

10.1016/s0016-5085(19)39775-6 ◽

2019 ◽

Vol 156 (6) ◽

pp. S-1124

Author(s):

Clara Caenepeel ◽

Sara Vieira-Silva ◽

Jorge F. Vázquez-Castellanos ◽

Bram Verstockt ◽

Marc Ferrante ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Gut Microbiota ◽

Treatment Response ◽

Bowel Disease ◽

Predictive Role ◽

Inflammatory Bowel

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The role of heme oxygenase and carbon monoxide in inflammatory bowel disease

Redox Report ◽

10.1179/174329210x12650506623889 ◽

2010 ◽

Vol 15 (5) ◽

pp. 193-201 ◽

Cited By ~ 20

Author(s):

Tomohisa Takagi ◽

Yuji Naito ◽

Kazuhiko Uchiyama ◽

Toshikazu Yoshikawa

Keyword(s):

Inflammatory Bowel Disease ◽

Carbon Monoxide ◽

Heme Oxygenase ◽

Bowel Disease ◽

Inflammatory Bowel

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Ethnic Differences in the Smoking-Related Risk of Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis

Journal of Crohn s and Colitis ◽

10.1093/ecco-jcc/jjab047 ◽

2021 ◽

Author(s):

Daniele Piovani ◽

Claudia Pansieri ◽

Soumya R R Kotha ◽

Amanda C Piazza ◽

Celia-Louise Comberg ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Latin American ◽

Bowel Disease ◽

Meta Analysis ◽

Study Data ◽

Future Research ◽

Related Risk ◽

Increased Risk ◽

Inflammatory Bowel

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.

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