The role of mycobiota-genotype association in inflammatory bowel diseases: a narrative review.
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ABSTRACT:
SUBMITTER: Mahmoudi E
PROVIDER: S-EPMC8106830 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundUlcerative colitis (UC) and Crohn disease (CD) are the 2 main types of inflammatory bowel diseases (IBDs). Several studies have been conducted to investigate the association of Glutathione S-Transferase M1 (GSTM1) null genotype with UC and CD, but the results are inconsistent. Here, we performed a meta-analysis to clarify this controversy based on relative large sample size.MethodsA systematic article searching was conducted in the PubMed, EMBASE, SCOPUS, WOS, ProQuest, Chinese National Knowledge Infrastructure (CNKI), and Chinese Wanfang databases up to August 31, 2019. Meta-analysis results were synthesized by using crude odds ratio (OR) with its 95% confidence interval (CI). Heterogeneity, sensitivity analysis, subgroup analysis, and publication bias were assessed by using STATA 11.0 software.ResultsA total of 15 relevant studies including 4353 IBDs patients (1848 CD cases, 2505 UC cases) and 5413 controls were included in this meta-analysis. Totally, we found a significant association between GSTM1 null genotype and risk to IBDs in the overall populations (OR = 1.37, 95%CI = 1.13-1.65, P = .001). Stratified by ethnicity, we found a significant association between GSTM1 null genotype and risk to IBDs in the Asian population (OR = 2.54, 95%CI = 2.15-3.00, P = .001), but not in the Caucasian population. Stratified by disease type, we found a significant association between GSTM1 null genotype with CD in the Asian population (OR = 2.37, 95%CI = 1.11-5.06, P = .026), and with UC in the Asian (OR = 2.48, 95%CI = 1.93-3.20, P = .001) population. In addition, funnel plot and Egger linear regression test suggests no publication bias in all genetic models.ConclusionGSTM1 null genotype is associated with susceptibility to IBD, UC, and CD in the Asian population. Further well-designed studies are still needed to confirm these findings.
| S-EPMC6946497 | biostudies-literature
Project description:Mitochondria are key cellular organelles whose main function is maintaining cell bioenergetics by producing ATP through oxidative phosphorylation. However, mitochondria are involved in a much higher number of cellular processes. Mitochondria are the home of key metabolic pathways like the tricarboxylic acid cycle and β-oxidation of fatty acids, as well as biosynthetic pathways of key products like nucleotides and amino acids, the control of the redox balance of the cell and detoxifying the cell from H2S and NH3. This plethora of critical functions within the cell is the reason mitochondrial function is involved in several complex disorders (apart from pure mitochondrial disorders), among them inflammatory bowel diseases (IBD). IBD are a group of chronic, inflammatory disorders of the gut, mainly composed of ulcerative colitis and Crohn's disease. In this review, we present the current knowledge regarding the impact of mitochondrial dysfunction in the context of IBD. The role of mitochondria in both intestinal mucosa and immune cell populations are discussed, as well as the role of mitochondrial function in mechanisms like mucosal repair, the microbiota- and brain-gut axes and the development of colitis-associated colorectal cancer.
| S-EPMC10707203 | biostudies-literature
Project description:Crohn's disease and ulcerative colitis, the major forms of inflammatory bowel diseases (IBD) in man, are complex diseases in which genetic and environmental factors interact to promote an excessive mucosal immune response directed against normal components of the bacterial microflora. There is also evidence that the pathologic process is due to defects in counter-regulatory mechanisms, such as those involving the immunosuppressive cytokine transforming growth factor (TGF)-β1. Indeed, studies in human IBD tissues and murine models of colitis have documented a disruption of TGF-β1 signalling marked by a block in the phosphorylation of Smad3, a signalling molecule associated with the activated TGF-β receptor, due to up-regulation of Smad7, an intracellular inhibitor of Smad3 phosphorylation. Knock-down of Smad7 with a specific antisense oligonucleotide restores TGF-β1/Smad3 signalling, thus resulting in a marked suppression of inflammatory cytokine production and attenuation of murine colitis. These findings together with the demonstration that Smad7 antisense oligonucleotide is not toxic when administered in mice have paved the way for the development of a Smad7 antisense oligonucleotide-based pharmaceutical compound that is now ready to enter the clinics. In this article we review the available data supporting the pathogenic role of Smad7 in IBD and discuss whether and how Smad7 antisense therapy could help dampen the ongoing inflammation in IBD.
| S-EPMC3484333 | biostudies-literature
Project description:BackgroundIndividuals with a history of depression/depressive symptoms are suspected to be at increased risk of incident inflammatory bowel diseases (IBDs).MethodsWe systematically searched MEDLINE/PubMed, Embase, and Scopus databases for longitudinal studies examining the association between depression/depressive symptoms and subsequent new-onset IBD (ie, Crohn's disease and ulcerative colitis). We included studies in which the exposure was a confirmed diagnosis of depression/depressive symptoms measured through a validated scale. To limit concerns of diagnostic bias and reverse causality, and support temporality between exposure and outcomes, we synthesized estimates corresponding to the longest time lag reported. Two authors extracted study data independently and assessed each study's risk of bias. Maximally adjusted relative risk (RR) estimates were synthesized using random- and fixed-effects models.ResultsOf 5307 records, 13 studies (8 cohort and 5 nested case-control studies; 9 million individuals) fulfilled the eligibility criteria. Depression was significantly associated with incident Crohn's disease (RRrandom, 1.17; 95% confidence interval, 1.02-1.34; 7 studies, 17 676 cases) and ulcerative colitis (RRrandom, 1.21; 95% confidence interval, 1.10-1.33; 6 studies, 28 165 cases). The primary studies considered pertinent confounders. Several years, on average, separated exposure and outcomes. No evidence of important heterogeneity or publication bias was found. Summary estimates were at low risk of bias, and results were confirmed in multiple sensitivity analyses. No firm conclusions could be drawn regarding a dilution of the association over time.ConclusionsIndividuals with a history of depression may show small-to-moderate increased risk of IBD even when depression is diagnosed several years before new-onset IBD. Further epidemiological and mechanistic studies should clarify whether these associations are causal.
| S-EPMC10988103 | biostudies-literature
Project description:an increased prevalence of gastro-duodenal ulceration was described almost sixty years ago as prodromal to idiopathic Parkinson's disease, while duodenal ulcers have been rarely diagnosed in patients with schizophrenia. The cytoprotective role of dopamine in animal models of gastrointestinal ulcerations has also been described. Interestingly, Parkinson's disease (PD) might share common pathophysiological links with inflammatory bowel disease (IBD) as epidemiological and genetic links already suggest. Thus, the aim of our study was to review the existing literature on the role of the gastrointestinal dopaminergic system in IBD pathogenesis and progression. a systematic search was conducted according to the PRISMA methodology. twenty-four studies satisfied the predetermined criteria and were included in our qualitative analysis. Due to different observations (cross-sectional studies) as well as experimental setups and applied methodologies (in vivo and in vitro studies) a meta-analysis could not be performed. No ongoing clinical trials with dopaminergic compounds in IBD patients were found. the impairment of the dopaminergic system seems to be a significant, yet underestimated, feature of IBD, and more in-depth observational studies are needed to further support the existing preclinical data.
| S-EPMC8657776 | biostudies-literature
Project description:Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality despite aggressive treatment of traditional risk factors. Chronic inflammation plays an important role in the initiation and progression of CVDs. Inflammatory bowel disease (IBD) is a systemic state of inflammation exhibiting increased levels of pro-inflammatory cytokines including tumour necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. Importantly, IBD is associated with increased risk for CVDs especially in women and young adults, including coronary artery disease, stroke, thromboembolic diseases, and arrhythmias. Potential mechanisms underlying the increased risk for CVDs in IBD patients include increased levels of inflammatory cytokines and oxidative stress, altered platelet function, hypercoagulability, decreased numbers of circulating endothelial progenitor cells, endothelial dysfunction, and possible interruption of gut microbiota. Although IBD does not appear to exacerbate the traditional risk factors for CVDs, including hypertension, hyperlipidaemia, diabetes mellitus, and obesity, aggressive risk stratifications are important for primary and secondary prevention of CVDs for IBD patients. Compared to 5-aminosalicylates and corticosteroids, anti-TNF-α therapy in IBD patients was consistently associated with decreasing cardiovascular events. In the absence of contraindications, low-dose aspirin and statins appear to be beneficial for IBD patients. Low-molecular-weight heparin is also recommended for patients who are hospitalized with acute IBD flares without major bleeding risk. A multidisciplinary team approach should be considered for the management of IBD patients.
| S-EPMC9242064 | biostudies-literature
Project description:Precise diagnostic biomarker in inflammatory bowel diseases (IBD) is still missing. We conducted a comprehensive overview of oxidative stress markers (OSMs) as potential diagnostic, differential, progression, and prognostic markers in IBD. A Pubmed, Web of Knowledge, and Scopus search of original articles on OSMs in IBD, published between January 2000 and April 2020, was conducted. Out of 874 articles, 79 eligible studies were identified and used to prepare the interpretative synthesis. Antioxidants followed by lipid peroxidation markers were the most popular and markers of oxidative DNA damage the least popular. There was a disparity in the number of retrieved papers evaluating biomarkers in the adult and pediatric population (n = 6). Of the reviewed OSMs, a promising performance has been reported for serum total antioxidant status as a mucosal healing marker, mucosal 8-OHdG as a progression marker, and for multi-analyte panels of lipid peroxidation products assessed non-invasively in breath as diagnostic and differential markers in the pediatric population. Bilirubin, in turn, was the only validated marker. There is a desperate need for non-invasive biomarkers in IBD which, however, will not be met in the near future by oxidative stress markers as they are promising but mostly at the early research phase of discovery.
| S-EPMC7459713 | biostudies-literature
Project description:Inflammatory bowel diseases are considered immune disorders with a complex genetic architecture involving constantly changing endogenous and exogenous factors. The rapid evolution of genomic technologies and the emergence of newly discovered molecular actors are compelling the research community to reevaluate the knowledge and molecular processes. The human intestinal tract contains intestinal human microbiota consisting of commensal, pathogenic, and symbiotic strains leading to immune responses that can contribute and lead to both systemic and intestinal disorders including IBD. In this review, we attempted to highlight some updates of the new IBD features related to genomics, microbiota, new emerging therapies and some major established IBD risk factors.
| S-EPMC9481278 | biostudies-literature
Project description:Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is associated with a loss or an imbalance of host-microbe interactions. Depletion-assisted deep metaproteomics was employed to reveal disease-specific networks of host-microbial protein associations in IBD.
2023-06-28 | PXD043380 |
Project description:ObjectivesThe inflammatory bowel diseases (IBDs) emerged after industrialization. We studied whether ambient air pollution levels were associated with the incidence of IBD.MethodsThe health improvement network (THIN) database in the United Kingdom was used to identify incident cases of Crohn's disease (n=367) or ulcerative colitis (n=591), and age- and sex-matched controls. Conditional logistic regression analyses assessed whether IBD patients were more likely to live in areas of higher ambient concentrations of nitrogen dioxide (NO(2)), sulfur dioxide (SO(2)), and particulate matter <10 ?m (PM(10)), as determined by using quintiles of concentrations, after adjusting for smoking, socioeconomic status, non-steroidal anti-inflammatory drugs (NSAIDs), and appendectomy. Stratified analyses investigated effects by age.ResultsOverall, NO(2), SO(2), and PM(10) were not associated with the risk of IBD. However, individuals ?23 years were more likely to be diagnosed with Crohn's disease if they lived in regions with NO(2) concentrations within the upper three quintiles (odds ratio (OR)=2.31; 95% confidence interval (CI)=1.25-4.28), after adjusting for confounders. Among these Crohn's disease patients, the adjusted OR increased linearly across quintile levels for NO(2) (P=0.02). Crohn's disease patients aged 44-57 years were less likely to live in regions of higher NO(2) (OR=0.56; 95% CI=0.33-0.95) and PM(10) (OR=0.48; 95% CI=0.29-0.80). Ulcerative colitis patients ?25 years (OR=2.00; 95% CI=1.08-3.72) were more likely to live in regions of higher SO(2); however, a dose-response effect was not observed.ConclusionsOn the whole, air pollution exposure was not associated with the incidence of IBD. However, residential exposures to SO(2) and NO(2) may increase the risk of early-onset ulcerative colitis and Crohn's disease, respectively. Future studies are needed to explore the age-specific effects of air pollution exposure on IBD risk.
| S-EPMC3180712 | biostudies-literature