Genetic and Epigenetic Etiology of Inflammatory Bowel Disease: An Update

Jarmakiewicz-Czaja, Sara; Zielińska, Magdalena; Sokal, Aneta; Filip, Rafał

doi:10.3390/genes13122388

Cited by 39 publications

(29 citation statements)

References 211 publications

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“…T reg cells play an important role in the suppression of inflammation through transforming-growth factor B (TGF-B), interleukine (IL) 35, and IL10. The deficiency of T reg cells leads to inflammation and IBD [33,[37][38][39]. Their role is important against Citrobacter rodentium and Salmonella enterica and was shown to be decreased in Bacteroides increased microbiome.…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

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Intestinal Microbiomics in Physiological and Pathological Conditions

Ionescu¹,

Cozma²,

Enache³

et al. 2024

Advances in Probiotics for Health and Nutrition

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Microbiomics represents a new science studying the microbiome, consisting of all the microorganisms of a given community. This new science collects data about all the members of the microbial community and quantifies the molecules responsible for the structure, function, and dynamics of the microbiome. The human microbiome plays a very important role in the healthy state and in a variety of disease states. The human microbiome knowledge has evolved during the last decades and nowadays one can consider that, in particular, the gut microbiota is seen as a significant organ holding 150 times more genes compared to the human genome. This chapter will focus on discussing the normal and modified phyla and species of the gut microbiome in a variety of conditions, providing a better understanding of host-microbiome interactions. We will highlight some new associations between intestinal dysbiosis and acute or chronic inflammatory and metabolic diseases.

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Section: Inflammatory Bowel Diseasementioning

confidence: 99%

“…Their role is important against Citrobacter rodentium and Salmonella enterica and was shown to be decreased in Bacteroides increased microbiome. Also, Clostridium clusters showed the ability to act on the differentiation of T reg cells [34,37,40,41].…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

Intestinal Microbiomics in Physiological and Pathological Conditions

Ionescu¹,

Cozma²,

Enache³

et al. 2024

Advances in Probiotics for Health and Nutrition

View full text Add to dashboard Cite

show abstract

“…Researchers have identified more than 230 genetic loci associated with IBD. These genes are primarily involved in major histocompatibility complex, pattern recognition, inflammation, and apoptosis [ 4 , 37 , 38 , 39 ]. Environmental risk factors relating to industrialization and excessive sanitation and hygiene have been reported.…”

Section: Introductionmentioning

confidence: 99%

Rosiglitazone Does Not Affect the Risk of Inflammatory Bowel Disease: A Retrospective Cohort Study in Taiwanese Type 2 Diabetes Patients

Tseng

2023

Pharmaceuticals

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Human studies on the effect of rosiglitazone on inflammatory bowel disease (IBD) are still lacking. We investigated whether rosiglitazone might affect IBD risk by using the reimbursement database of Taiwan’s National Health Insurance to enroll a propensity-score-matched cohort of ever users and never users of rosiglitazone. The patients should have been newly diagnosed with diabetes mellitus between 1999 and 2006 and should have been alive on 1 January 2007. We then started to follow the patients from 1 January 2007 until 31 December 2011 for a new diagnosis of IBD. Propensity-score-weighted hazard ratios were estimated with regards to rosiglitazone exposure in terms of ever users versus never users and in terms of cumulative duration and cumulative dose of rosiglitazone therapy for dose–response analyses. The joint effects and interactions between rosiglitazone and risk factors of psoriasis/arthropathies, dorsopathies, and chronic obstructive pulmonary disease/tobacco abuse and the use of metformin were estimated by Cox regression after adjustment for all covariates. A total of 6226 ever users and 6226 never users were identified and the respective numbers of incident IBD were 95 and 111. When we compared the risk of IBD in ever users to that of the never users, the estimated hazard ratio (0.870, 95% confidence interval: 0.661–1.144) was not statistically significant. When cumulative duration and cumulative dose of rosiglitazone therapy were categorized by tertiles and hazard ratios were estimated by comparing the tertiles of rosiglitazone exposure to the never users, none of the hazard ratios reached statistical significance. In secondary analyses, rosiglitazone has a null association with Crohn’s disease, but a potential benefit on ulcerative colitis (UC) could not be excluded. However, because of the low incidence of UC, we were not able to perform detailed dose–response analyses for UC. In the joint effect analyses, only the subgroup of psoriasis/arthropathies (-)/rosiglitazone (-) showed a significantly lower risk in comparison to the subgroup of psoriasis/arthropathies (+)/rosiglitazone (-). No interactions between rosiglitazone and the major risk factors or metformin use were observed. We concluded that rosiglitazone has a null effect on the risk of IBD, but the potential benefit on UC awaits further investigation.

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“…Numerous genes have been identified as initiating or driving the pathogenesis of IBD and thus influencing intestinal homeostasis [ 9 , 10 ]. These genes include, but are not limited to, cytokine factors (TNF-α, IL-10), cytokine receptors (IL-17R and IL-23R), transcription factors (NFκB and JAK/STAT pathway), kinases (PTPN22, Tyk2, RIPK2), apoptotic elements (CARD9 and caspase 11), and elements involved in autophagic signaling (ATG16L, IRGM, NOD2) [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Novel Biomarkers for Inflammatory Bowel Disease and Colorectal Cancer: An Interplay between Metabolic Dysregulation and Excessive Inflammation

Salla

Guo

Joshi

et al. 2023

IJMS

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Persistent inflammation can trigger altered epigenetic, inflammatory, and bioenergetic states. Inflammatory bowel disease (IBD) is an idiopathic disease characterized by chronic inflammation of the gastrointestinal tract, with evidence of subsequent metabolic syndrome disorder. Studies have demonstrated that as many as 42% of patients with ulcerative colitis (UC) who are found to have high-grade dysplasia, either already had colorectal cancer (CRC) or develop it within a short time. The presence of low-grade dysplasia is also predictive of CRC: Many signaling pathways are shared among IBD and CRC, including cell survival, cell proliferation, angiogenesis, and inflammatory signaling pathways. Current IBD therapeutics target a small subset of molecular drivers of IBD, with many focused on the inflammatory aspect of the pathways. Thus, there is a great need to identify biomarkers of both IBD and CRC, that can be predictive of therapeutic efficacy, disease severity, and predisposition to CRC. In this study, we explored the changes in biomarkers specific for inflammatory, metabolic, and proliferative pathways, to help determine the relevance to both IBD and CRC. Our analysis demonstrated, for the first time, the loss of the tumor suppressor protein Ras associated family protein 1A (RASSF1A), via epigenetic changes, the hyperactivation of the obligate kinase of the NOD2 pathogen recognition receptor (receptor interacting protein kinase 2 [RIPK2]), the loss of activation of the metabolic kinase, AMP activated protein kinase (AMPKα1), and, lastly, the activation of the transcription factor and kinase Yes associated protein (YAP) kinase, that is involved in proliferation of cells. The expression and activation status of these four elements are mirrored in IBD, CRC, and IBD-CRC patients and, importantly, in matched blood and biopsy samples. The latter would suggest that biomarker analysis can be performed non-invasively, to understand IBD and CRC, without the need for invasive and costly endoscopic analysis. This study, for the first time, illustrates the need to understand IBD or CRC beyond an inflammatory perspective and the value of therapeutics directed to reset altered proliferative and metabolic states within the colon. The use of such therapeutics may truly drive patients into remission.

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Genetic and Epigenetic Etiology of Inflammatory Bowel Disease: An Update

Cited by 39 publications

References 211 publications

Intestinal Microbiomics in Physiological and Pathological Conditions

Intestinal Microbiomics in Physiological and Pathological Conditions

Rosiglitazone Does Not Affect the Risk of Inflammatory Bowel Disease: A Retrospective Cohort Study in Taiwanese Type 2 Diabetes Patients

Novel Biomarkers for Inflammatory Bowel Disease and Colorectal Cancer: An Interplay between Metabolic Dysregulation and Excessive Inflammation

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