scholarly journals Intestinal Taxa Abundance and Diversity in Inflammatory Bowel Disease Patients: An Analysis including Covariates and Confounders

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 260
Author(s):  
Adelaide Teofani ◽  
Irene Marafini ◽  
Federica Laudisi ◽  
Daniele Pietrucci ◽  
Silvia Salvatori ◽  
...  
Keyword(s):  
Dairy Products ◽  
Dietary Habits ◽  
Rrna Gene ◽  
Disease Extent ◽  
Intestinal Dysbiosis ◽  
Gene Sequence Analysis ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Abundance And Diversity ◽  
The Impact

Intestinal dysbiosis has been widely documented in inflammatory bowel diseases (IBDs) and is thought to influence the onset and perpetuation of gut inflammation. However, it remains unclear whether such bacterial changes rely in part on the modification of an IBD-associated lifestyle (e.g., smoking and physical activity) and diet (e.g., rich in dairy products, cereals, meat and vegetables). In this study, we investigated the impact of these habits, which we defined as confounders and covariates, on the modulation of intestinal taxa abundance and diversity in IBD patients. 16S rRNA gene sequence analysis was performed using genomic DNA extracted from the faecal samples of 52 patients with Crohn’s disease (CD) and 58 with ulcerative colitis (UC), which are the two main types of IBD, as well as 42 healthy controls (HC). A reduced microbial diversity was documented in the IBD patients compared with the HC. Moreover, we identified specific confounders and covariates that influenced the association between some bacterial taxa and disease extent (in UC patients) or behaviour (in CD patients) compared with the HC. In particular, a PERMANOVA stepwise regression identified the variables “age”, “eat yogurt at least four days per week” and “eat dairy products at least 4 days per week” as covariates when comparing the HC and patients affected by ulcerative proctitis (E1), left-sided UC (distal UC) (E2) and extensive UC (pancolitis) (E3). Instead, the variables “age”, “gender”, “eat meat at least four days per week” and “eat bread at least 4 days per week” were considered as covariates when comparing the HC with the CD patients affected by non-stricturing, non-penetrating (B1), stricturing (B2) and penetrating (B3) diseases. Considering such variables, our analysis indicated that the UC extent differentially modulated the abundance of the Bifidobacteriaceae, Rikenellaceae, Christensenellaceae, Marinifilaceae, Desulfovibrionaceae, Lactobacillaceae, Streptococcaceae and Peptostreptococcaceae families, while the CD behaviour influenced the abundance of Christensenellaceae, Marinifilaceae, Rikenellaceae, Ruminococcaceae, Barnesiellaceae and Coriobacteriaceae families. In conclusion, our study indicated that some covariates and confounders related to an IBD-associated lifestyle and dietary habits influenced the intestinal taxa diversity and relative abundance in the CD and UC patients compared with the HC. Indeed, such variables should be identified and excluded from the analysis to characterize the bacterial families whose abundance is directly modulated by IBD status, as well as disease extent or behaviour.

scholarly journals Inflammatory Bowel Diseases: Host-Microbial-Environmental Interactions in Dysbiosis

Diseases ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 13
Author(s):  
Catherine Colquhoun ◽  
Michelle Duncan ◽  
George Grant
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Early Life ◽  
Secretory Iga ◽  
Mucus Production ◽  
Functional Changes ◽  
Environmental Interactions ◽  
Intestinal Dysbiosis ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Abundance And Diversity

Crohn’s Disease (CD) and Ulcerative Colitis (UC) are world-wide health problems in which intestinal dysbiosis or adverse functional changes in the microbiome are causative or exacerbating factors. The reduced abundance and diversity of the microbiome may be a result of a lack of exposure to vital commensal microbes or overexposure to competitive pathobionts during early life. Alternatively, many commensal bacteria may not find a suitable intestinal niche or fail to proliferate or function in a protective/competitive manner if they do colonize. Bacteria express a range of factors, such as fimbriae, flagella, and secretory compounds that enable them to attach to the gut, modulate metabolism, and outcompete other species. However, the host also releases factors, such as secretory IgA, antimicrobial factors, hormones, and mucins, which can prevent or regulate bacterial interactions with the gut or disable the bacterium. The delicate balance between these competing host and bacteria factors dictates whether a bacterium can colonize, proliferate or function in the intestine. Impaired functioning of NOD2 in Paneth cells and disrupted colonic mucus production are exacerbating features of CD and UC, respectively, that contribute to dysbiosis. This review evaluates the roles of these and other the host, bacterial and environmental factors in inflammatory bowel diseases.

scholarly journals The impact of selected food additives on the gastrointestinal tract in the example of nonspecific inflammatory bowel diseases

2021 ◽  
Author(s):  
Sara Jarmakiewicz - Czaja ◽  
Dominika Piątek ◽  
Rafał Filip
Keyword(s):  
Gastrointestinal Tract ◽  
Food Industry ◽  
Intestinal Microflora ◽  
Food Additives ◽  
Cytotoxic Effects ◽  
Intestinal Dysbiosis ◽  
Food Dyes ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
The Impact

Various types of food additives are widely used in the food industry. Due to their properties extending the usefulness for consuming food products, they give them different colours, consistency, or taste. The products are marked ‘E’ and the code is assigned to the subscription used. Many of the supplements affect human health negatively. Emulsifiers or stabilizers can lead to epithelial loads and the development of inflammation. Sucrose and other sweeteners may change the composition of the intestinal microflora and thus lead to intestinal blockage. Some additives classified as preservatives are available and may predispose to intestinal dysbiosis. Available substances belonging to food dyes may predispose to genotoxic and cytotoxic effects and cause inflammation in the intestines. Substances added to food can also cause disorders of intestinal homeostasis.

scholarly journals Intestinal microbiota changes induced by TNF-inhibitors in IBD-related spondyloarthritis

RMD Open ◽  
2021 ◽  
Vol 7 (3) ◽  
pp. e001755
Author(s):  
Maria Chiara Ditto ◽  
Simone Parisi ◽  
Gianpiero Landolfi ◽  
Richard Borrelli ◽  
Cristina Realmuto ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
16S Rrna Gene Sequencing ◽  
Rrna Gene ◽  
Biological Drugs ◽  
Alpha And Beta Diversity ◽  
Close Relationship ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Rrna Gene Sequencing ◽  
The Impact

BackgroundThe close relationship between joints and gut inflammation has long been known and several data suggest that dysbiosis could link spondyloarthritis (SpA) to inflammatory bowel diseases (IBD). The introduction of biological drugs, in particular tumour necrosis factor inhibitors (TNFi), revolutionised the management of both these diseases. While the impact of conventional drugs on gut microbiota is well known, poor data are available about TNFi.AimTo investigate the impact of TNFi on gut microbiota.MethodsWe evaluated 20 patients affected by enteropathic arthritis, naïve for biological drugs, treated with TNFi at baseline and after 6 months of therapy. All patients followed a Mediterranean diet. Patients performed self-sampling of a faecal sample at baseline and after 6 months of therapy. NGS-based ITS and 16S rRNA gene sequencing was performed, followed by the taxonomic bioinformatics analysis.ResultsAfter 6 months of therapy, we detected a remarkable increase in Lachnospiraceae family (Δ +10.3, p=0.04) and Coprococcus genus (Δ +2.8, p=0.003). We also noted a decreasing trend in Proteobacteria (Δ −8.0, p=0.095) and Gammaproteobacteria (Δ −9, p=0.093) and an increasing trend in Clostridia (Δ +8.2, p=0.083). We did not find differences between TNFi responders (SpA improvement or IBD remission achieved) and non-responders in terms of alpha and beta diversity.ConclusionsOur findings are consistent with the hypothesis that TNFi therapy tends to restore the intestinal eubiosis.

Localization and Activity of Inflammatory Bowel Disease Using 111ln Leukocyte Imaging

1988 ◽  
Vol 27 (03) ◽  
pp. 83-86 ◽  
Author(s):  
B. Briele ◽  
F. Wolf ◽  
H. J. Biersack ◽  
F. F. Knapp ◽  
A. Hotze
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Disease Activity ◽  
Bowel Disease ◽  
Cell Uptake ◽  
Disease Extent ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Leukocyte Imaging

A prospective study was initiated to compare the clinically proven results concerning localization/extent and activity of inflammatory bowel diseases with those of 111ln-oxine leukocyte imaging. All patients studied were completely examined with barium enema x-ray, clinical and laboratory investigations, and endoscopy with histopathology. A total of 31 leukocyte scans were performed in 15 patients (12 with Crohn’s disease, 3 with ulcerative colitis). The scans were graded by comparing the cell uptake of a lesion (when present) and a bone marrow area providing a count ratio (CR). The inflammatory lesions were correctly localized on 26 leukocyte scans, and in 21 scans the scintigraphically estimated extent of disease was identical to endoscopy. In 5 cases the disease extent was underestimated, 4 scans in patients with relapse of Crohn’s disease were falsely negative, and in one patient with remission truly negative. The scintigraphically assessed disease activity was also in a good agreement with clinical disease activity based on histopathology in all cases. We conclude that leukocyte imaging provides valuable information about localization and activity of inflammatory bowel disease.

scholarly journals Stiffness Regulates Intestinal Stem Cell Fate

2021 ◽  
Author(s):  
Shijie He ◽  
Peng Lei ◽  
Wenying Kang ◽  
Priscilla Cheung ◽  
Tao Xu ◽  
...  
Keyword(s):  
Cell Fate ◽  
Nuclear Translocation ◽  
Goblet Cells ◽  
Metabolic Phenotype ◽  
Hydrogel Matrix ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
The Impact

SummaryDoes fibrotic gut stiffening caused by inflammatory bowel diseases (IBD) direct the fate of intestinal stem cells (ISCs)? To address this question we first developed a novel long-term culture of quasi-3D gut organoids plated on hydrogel matrix of varying stiffness. Stiffening from 0.6kPa to 9.6kPa significantly reduces Lgr5high ISCs and Ki67+ progenitor cells while promoting their differentiation towards goblet cells. These stiffness-driven events are attributable to YAP nuclear translocation. Matrix stiffening also extends the expression of the stemness marker Olfactomedin 4 (Olfm4) into villus-like regions, mediated by cytoplasmic YAP. We next used single-cell RNA sequencing to generate for the first time the stiffness-regulated transcriptional signatures of ISCs and their differentiated counterparts. These signatures confirm the impact of stiffening on ISC fate and additionally suggest a stiffening-induced switch in metabolic phenotype, from oxidative phosphorylation to glycolysis. Finally, we used colon samples from IBD patients as well as chronic colitis murine models to confirm the in vivo stiffening-induced epithelial deterioration similar to that observed in vitro. Together, these results demonstrate stiffness-dependent ISC reprograming wherein YAP nuclear translocation diminishes ISCs and Ki67+ progenitors and drives their differentiation towards goblet cells, suggesting stiffening as potential target to mitigate gut epithelial deterioration during IBD.

scholarly journals P261 Systematic review with meta-analysis: The impact of concomitant immune-mediated diseases on the disease course of inflammatory bowel disease

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S280-S281
Author(s):  
M Attauabi ◽  
M Zhao ◽  
F Bendtsen ◽  
J Burisch
Keyword(s):  
Biologic Therapy ◽  
Meta Analysis ◽  
Multidisciplinary Care ◽  
Disease Course ◽  
Immune Mediated ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Meta Analyses ◽  
The Impact

Abstract Background Several studies have shown an association between inflammatory bowel diseases [IBD] and immune-mediated diseases [IMIDs], but data on the impact of co-occurring IMIDs on IBD course are inconsistent. The aim of this study was to investigate the impact of co-occurring IMIDs on IBD phenotype and disease course. Methods PubMed and EMBASE were searched from database inception through December 2018 and updated in October 2019 for studies reporting prevalences or odds, risks or hazard ratios of IBD-related disease outcomes in patients with and without co-existing IMIDs. Meta-analyses were performed to estimate summary prevalences and risks of the outcomes which included disease extension, IBD-related surgery and hospitalisation, malignancy, mortality and need of medication (biologic therapy, steroids and immunomodulators). IMIDs were stratified into primary sclerosing cholangitis [PSC] and ‘IMIDs other than PSC’. Results A total of 93 studies comprising 14,307 IBD patients with IMIDs and 3,409,914 IBD patients without IMIDs were included in the study. Summary risks and prevalences with 95% confidence intervals for each outcome are presented in figures 1 and 2, respectively. The following results are all significant (p < 0.05). Compared with patients without co-occurring IMIDs, patients with ulcerative colitis [UC] and co-occurring IMIDs other than PSC more frequently received immunomodulators and steroids, and patients with Crohn’s disease [CD] and concomitant IMIDs other than PSC more often received biologic therapy. UC patients with co-existing IMIDs other than PSC more often underwent IBD-related surgery, while patients with CD and PSC received fewer surgeries. In addition, UC patients with co-occurring PSC were at increased risk for having extensive colitis, pancolitis, and malignancies. Patients with UC and PSC had a higher mortality rate, but no difference was found among patients with IMIDs other than PSC. PSC did not influence hospitalisation rates among IBD patients. Conclusion This meta-analysis found that IBD patients with co-existing IMIDs have a different disease course than patients without concomitant IMIDs. This study emphasises the importance of multidisciplinary care of IBD and that physicians caring for IBD patients need to be aware of IMIDs as a prognostic factor.

scholarly journals Dynamic, Transient, and Robust Increase in the Innervation of the Inflamed Mucosa in Inflammatory Bowel Diseases

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2253
Author(s):  
Miguel Gonzalez Acera ◽  
Marvin Bubeck ◽  
Fabrizio Mascia ◽  
Leonard Diemand ◽  
Gregor Sturm ◽  
...  
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Inflammatory Bowel Diseases ◽  
Cell Activation ◽  
Immune Cell ◽  
Bowel Diseases ◽  
Treatment Naïve ◽  
Inflammatory Bowel ◽  
Molecular Patterns ◽  
The Impact

Inflammatory bowel diseases (IBD) are characterized by chronic dysregulation of immune homeostasis, epithelial demise, immune cell activation, and microbial translocation. Each of these processes leads to proinflammatory changes via the release of cytokines, damage-associated molecular patterns (DAMPs), and pathogen-associated molecular patterns (PAMPs), respectively. The impact of these noxious agents on the survival and function of the enteric nervous system (ENS) is poorly understood. Here, we show that in contrast to an expected decrease, experimental as well as clinical colitis causes an increase in the transcript levels of enteric neuronal and glial genes. Immunostaining revealed an elevated neuronal innervation of the inflamed regions of the gut mucosa. The increase was seen in models with overt damage to epithelial cells and models of T cell-induced colitis. Transcriptomic data from treatment naïve pediatric IBD patients also confirmed the increase in the neuroglial genes and were replicated on an independent adult IBD dataset. This induction in the neuroglial genes was transient as levels returned to normal upon the induction of remission in both mouse models as well as colitis patients. Our data highlight the dynamic and robust nature of the enteric nervous system in colitis and open novel questions on its regulation.

scholarly journals Vitamin D Modulates Intestinal Microbiota in Inflammatory Bowel Diseases

2020 ◽  
Author(s):  
Carolina Battistini ◽  
Rafael Ballan ◽  
Marcos Herkenhoff ◽  
Susana Saad ◽  
Jun Sun
Keyword(s):  
Vitamin D ◽  
Gut Microbiota ◽  
Immune Cell ◽  
Vitamin D Supplementation ◽  
Dihydroxyvitamin D3 ◽  
Intestinal Dysbiosis ◽  
Bowel Diseases ◽  
Intestine Mucosa ◽  
Transmural Inflammation ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic disease in the gastrointestinal tract (GIT). IBD include ulcerative colitis (UC), which generally affects only the large intestine mucosa and submucosa, and Crohn’s disease (CD), which may affect any part of the GIT by transmural inflammation. Both UC and CD are associated with an imbalance of the gut microbiota composition and injuries in the intestinal mucosa. The intestinal dysbiosis is related to a reduction in butyrate-producing species, impairing the anti-inflammatory response of the immune system, and is commonly associated with micronutrients deficiency, e.g. vitamin D hypovitaminosis. Vitamin D is involved in several critical functions, including immune cell differentiation, regulation of microbiota, gene transcription, and barrier integrity. Vitamin D supplementation in IBD patients showed promising results in reducing the disease activity and modulating gut microbiota. Vitamin D receptor (VDR) regulates the biological actions of the active vitamin D metabolite, 1α,25-dihydroxyvitamin D3. Evidence supports that the VDR signaling is involved in the genetic, environmental, immune, and microbial aspects of IBD. Low VDR expression and dysfunction of vitamin D/VDR signaling are reported in IBD patients. Vitamin D/VDR deficiency could be considered as a multifunctional susceptibility factor in IBD. Therefore, in this review, we will discuss the progress in clinical studies, mechanism studies on Vitamin D /VDR, and potential use of vitamin D supplementation as adjuvant therapy to restore gut microbiota balance, promote beneficial metabolites, and inhibit inflammation status in patients with IBD.

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