Pathogenesis Of Inflammatory Bowel Disease Research Articles

Comparison of microbial communities and the profile of sulfate-reducing bacteria in patients with ulcerative colitis and their association with bowel diseases: a pilot study.

Considerable evidence has accumulated regarding the molecular relationship between gut microbiota (GM) composition and the onset (clinical presentation and prognosis of ulcerative colitis (UC)). In addition, it is well documented that short-chain fatty acid (SCFA)-producing bacteria may play a fundamental role in maintaining an anti-inflammatory intestinal homeostasis, but sulfate- and sulfite reducing bacteria may be responsible for the production of toxic metabolites, such as hydrogen sulfide and acetate. Hence, the present study aimed to assess the GM composition - focusing on sulfate-reducing bacteria (SRB) - in patients with severe, severe-active and moderate UC. Each one of the six enrolled patients provided two stool samples in the following way: one sample was cultivated in a modified SRB-medium before 16S rRNA sequencing and the other was not cultivated. Comparative phylogenetic analysis was conducted on each sample. Percentage of detected gut microbial genera showed considerable variation based on the patients' disease severity and cultivation in the SRB medium. In detail, samples without cultivation from patients with moderate UC showed a high abundance of the genera Bacteroides, Bifidobacterium and Ruminococcus, but after SRB cultivation, the dominant genera were Bacteroides, Klebsiella and Bilophila. On the other hand, before SRB cultivation, the main represented genera in patients with severe UC were Escherichia-Shigella, Proteus, Methanothermobacter and Methanobacterium. However, after incubation in the SRB medium Bacteroides, Proteus, Alistipes and Lachnoclostridium were predominant. Information regarding GM compositional changes in UC patients may aid the development of novel therapeutic strategies (e.g., probiotic preparations containing specific bacterial strains) to counteract the mechanisms of virulence of harmful bacteria and the subsequent inflammatory response that is closely related to the pathogenesis of inflammatory bowel diseases.

Aryl hydrocarbon receptor confers protection against macrophage pyroptosis and intestinal inflammation through regulating polyamine biosynthesis.

Rationale: The aryl hydrocarbon receptor (AhR) functions in the regulation of intestinal inflammation, but knowledge of the underlying mechanisms in innate immune cells is limited. Here, we investigated the role of AhR in modulating the functions of macrophages in inflammatory bowel disease pathogenesis. Methods: The cellular composition of intestinal lamina propria CD45+ leukocytes in a dextran sulfate sodium (DSS)-induced mouse colitis model was determined by single-cell RNA sequencing. Macrophage pyroptosis was quantified by analysis of lactate dehydrogenase release, propidium iodide staining, enzyme-linked immunosorbent assay, western blot, and flow cytometry. Differentially expressed genes were confirmed by RNA-seq, RT-qPCR, luciferase assay, chromatin immunoprecipitation, and immunofluorescence staining. Results: AhR deficiency mediated dynamic remodeling of the cellular composition of intestinal lamina propria (LP) CD45+ immune cells in a colitis model, with a significant increase in monocyte-macrophage lineage. Mice with AhR deficiency in myeloid cells developed more severe dextran sulfate sodium induced colitis, with concomitant increased macrophage pyroptosis. Dietary supplementation with an AhR pre-ligand, indole-3-carbinol, conferred protection against colitis while protection failed in mice lacking AhR in myeloid cells. Mechanistically, AhR signaling inhibited macrophage pyroptosis by promoting ornithine decarboxylase 1 (Odc1) transcription, to enhance polyamine biosynthesis. The increased polyamine, particularly spermine, inhibited NLRP3 inflammasome assembly and subsequent pyroptosis by suppressing K+ efflux. AHR expression was positively correlated with ODC1 in intestinal mucosal biopsies from patients with ulcerative colitis. Conclusions: These findings suggest a functional role for the AhR/ODC1/polyamine axis in maintaining intestinal homeostasis, providing potential targets for treatment of inflammatory bowel disease.

The association between psoriasis, psoriasis severity, and inflammatory bowel disease: a population-based analysis.

The skin-gut axis, characterized by bidirectional communication between the skin and gut, plays a crucial role in the pathogenesis of psoriasis and inflammatory bowel diseases (IBD). We aimed to explore the association between psoriasis and IBD and identify predictors associated with IBD development among patients with psoriasis. Retrospective cohort study. A retrospective study which utilized an electronic database from the Meuhedet Health Maintenance Organization (MHMO) in Israel. Psoriasis was categorized as severe if any systemic agent or phototherapy was administered. Univariate and multivariate logistic regressions were used to identify specific predictors for IBD, with adjustments made for potential confounders. The study received approval from the Ethical Committee of the MHMO. In total, 61,003 adult patients who were diagnosed with psoriasis between 2000 and 2022 were included. Among them, 1495/61,003 patients (2.4%) were diagnosed with IBD, as compared to 3834/244,012 patients (1.6%) in the non-psoriasis group [adjusted odds ratio (OR): 1.47; 95% confidence interval (CI): 1.37-1.56; p < 0.001]. Increased age (OR: 1.01; 95% CI: 1.01-1.02; p < 0.001), male gender (OR: 1.22; 95% CI: 1.03-1.45; p = 0.024), and Jewish ethnicity (OR: 2.5; 95% CI: 1.2-4.1; p < 0.001) were identified as significant risk factors for IBD. Spondyloarthropathies, including psoriatic arthritis (OR: 2.27; 95% CI: 1.86-2.77; p < 0.001) and ankylosing spondylitis (OR: 2.82; 95% CI: 1.5-5.32; p < 0.05), were associated with a higher prevalence of IBD. Furthermore, severe psoriasis was significantly associated with a higher likelihood of IBD, compared to mild psoriasis (OR: 16.03; 95% CI: 11.02-23.34; p < 0.001). A significant association between psoriasis and IBD was demonstrated, including its subtypes: Crohn's disease and ulcerative colitis. Moreover, such association may depend on psoriasis severity as determined by the treatment used. This association warrants further investigation and implies a potential need for closer monitoring of patients with severe psoriasis.

Glycoprotein 2 as a gut gate keeper for mucosal equilibrium between inflammation and immunity.

Glycoprotein 2 (GP2) is a widely distributed protein in the digestive tract, contributing to mucosal barrier maintenance, immune homeostasis, and antigen-specific immune response, while also being linked to inflammatory bowel disease (IBD) pathogenesis. This review sheds light on the extensive distribution of GP2 within the gastrointestinal tract and its intricate interplay with the immune system. Furthermore, the significance of GP2 autoantibodies in diagnosing and categorizing IBD is underscored, alongside the promising therapeutic avenues for modulating GP2 to regulate immunity and maintain mucosal balance.

D-Mannose promotes recovery from experimental colitis by inducing AMPK phosphorylation to stimulate epithelial repair.

Delayed mucosal healing and impaired intestinal epithelial barrier function have been implicated in the pathogenesis of ulcerative colitis (UC). Accordingly, restoration of epithelial barrier function as a means to reshape mucosal homeostasis represents an important strategy for use in the treatment of UC. In this study, we examined the role and mechanisms of D-mannose in the recovery of colitis as assessed in both animal and cell models. We found that D-mannose ameliorated inflammation, promoted mucosal healing in the colon and therefore was able to induce the recovery of UC. Furthermore, D-mannose increased the expression of tight junction (TJ) proteins and reduced the intestinal permeability during the recovery of colitis. Moreover, D-mannose inhibited M1 macrophage polarization and promoted M2 macrophage polarization via inducing AMPK phosphorylation while reducing mTOR phosphorylation in both models. In addition, increased TJ protein expression and decreased paracellular permeability were observed in NCM460 cells when incubated with the supernatants of D-mannose-treated RAW264.7 cells, suggesting that M1/M2 polarization induced by D-mannose modulates the expression of TJ proteins. Further study showed that D-mannose significantly upregulated the expression of TJ proteins in DSS-treated NCM460 cells by inducing AMPK phosphorylation, indicating a direct protective effect on epithelial cells. Finally, the protective effects of D-mannose were significantly abrogated by the presence of compound C, an AMPK inhibitor. Taken together, our data indicate that D-mannose can alleviate inflammation and foster epithelial restitution in UC recovery by inducing the TJ protein expression, which are achieved by inducing AMPK phosphorylation in the epithelium and/or macrophages.

The Role of Akkermansia muciniphila and Faecalibacterium prausnitzii in the Pathogenesis of Ulcerative Colitis and Crohn's Disease.

Crohn's disease (CD) and ulcerative colitis (UC) are inflammatory bowel diseases with uncertain etiology. We aimed to determine the amounts of Akkermansia muciniphila and Faecalibacterium prausnitzii in the intestinal microbiota of these patients and to correlate their amounts with blood IL-8, IL-10, and IL-12 cytokine levels. Thirty UC, 30 CDs, and 46 healthy controls were included. IL-8, IL-10, and IL-12 levels of blood samples were analyzed by ELISA. The amounts of Akkermansia muciniphila and Faecalibacterium prausnitzii were determined by the LightCycler 480 qPCR system. F. prausnitzii, A. muciniphila, IL-10, and IL-12 decreased in patient groups, while IL-8 decreased in UC but increased in CD. A significant difference was detected between the patient and control groups in terms of F. prausnitzii, A. muciniphila, and IL-8, but not for others. The amount of F. prausnitzii was correlated with IL-8 and IL-10 in UC and with IL-10 in CD patients. The decrease in the amount of F. prausnitzii was associated with the increase in UC disease severity. A. muciniphila and F. prausnitzii were detected in lower amounts in both diseases. F. prausnitzii decreased more with the severity of UC, suggesting that these bacteria may have complex roles in their etiopathogenesis.

Probiotics in the Treatment of Inflammatory Bowel Diseases.

Inflammatory bowel diseases (IBD) are chronic, incurable inflammatory condition of the gut. They comprise Crohn's disease and ulcerative colitis. Crohn's disease (CD) may affect any tract of the gastrointestinal (GI) tract and is a transmural inflammatory condition; ulcerative colitis (UC), on the other hand, is limited to the mucosal layer of the rectum and colon. Treatment options available for both IBD are notoriously loaded with potentially serious side effects and risks. Although the pathogenesis of IBD involves a complex interaction between genetic, environmental, microbial and immunological factors, there is evidence that the interplay between the microbiota and the GI mucosa has a preponderant role. It is therefore no surprise that in recent years, a growing interest for effective and safer alternatives has focused on the potential role of prebiotics and-especially-probiotics.The mechanisms of action underlying the potential benefits of probiotics in IBD have been largely and quite extensively investigated in vitro and in vivo experiments. In terms of clinical evidence, the results of trials in the induction of remission of active CD or the maintenance of its remission with probiotics have been so far largely disappointing, to the point that their use in this disease cannot be at present recommended.On the contrary, for the treatment as well as for maintenance therapy of UC, there is clinical evidence of efficacy for some specific strains or multi-strain preparations.It is evident that this is a rapidly evolving and promising field; more data are very likely to yield a better understanding on what strains and in what doses should be used in different specific clinical settings, as we expect new and exciting developments of precision and even personalized therapy by the fast-growing field of probiogenomics.

Discerning Endoscopic Severity of Inflammatory Bowel Disease by Scoping the Peripheral Blood Transcriptome

Background and AimsUlcerative colitis (UC) and Crohn’s disease (CD) are chronic inflammatory bowel diseases (IBD) with an incompletely understood etiology and pathogenesis. Identification of suitable drug targets and assessment of disease severity are crucial for optimal management. MethodsUsing RNA-sequencing, we investigated differential gene expression in peripheral blood samples from IBD-patients and non-inflamed controls, analysed pathway enrichment, and identified genes whose expression correlated with endoscopic disease severity. ResultsNeutrophil degranulation emerged as the most significant pathway across all IBD sample types. Signalling by interleukins was prominent in patients with active intestinal inflammation, but also enriched in CD and UC patients without intestinal inflammation. Nevertheless, genes correlated to endoscopic disease severity implicated the primary cilium in CD patients, and translation and focal adhesion in UC patients. Moreover, several of these genes were located in genome-wide associated loci linked to IBD, cholesterol levels, blood cell counts, and levels of markers assessing liver and kidney function. These genes also suggested connections to intestinal epithelial barrier dysfunction, contemporary IBD drug treatment, and new actionable drug targets. A large number of genes associated with endoscopic disease severity corresponded to non-coding RNAs. ConclusionsThis study revealed biological pathways associated with IBD disease state and endoscopic disease severity, thus providing insights into the underlying mechanisms of IBD pathogenesis as well as identifying potential biomarkers and therapies. Peripheral blood might constitute a suitable non-invasive diagnostic sample type, in which gene expression profiles might serve as indicators of ongoing mucosal inflammation, and thus guide personalized treatment decisions.

The Role of Microcin B17-Producing Escherichia Coli, Isolated from Patients with Inflammatory Bowel Disease on Rat Intestine

Background: Inflammatory Bowel Disease (IBD) is a chronic gastrointestinal disease, Crohn’s disease (CD) and ulcerative colitis (UC) are two distinct kinds of IBD. Recent researches have linked between Escherichia coli which produce the toxin microcin B17 (E. coli/+mB17) and the development of inflammatory bowel disease (IBD). Objective: This study aimed to demonstrate the relationship between these E. coli isolates and the emergence of IBD in an experimental animal models. Materials and Methods: Twenty female rats, five-weeks-old were divided in to four groups; first group, were orally given E. coli/+mB17 isolated from crohn’s patients stool, the second group rats were orally given E. coli/+mB17 isolated from patients stool with ulcerative colitis, in the third group were orally given E. coli non-producing microcin B17 (E. coli/-mB17) isolated from patients stool with IBD, and the last group received normal saline orally, as control. After fifteen weeks of administration, Blood was drawn for serological tests which include interlukin-10 (IL-10) and tumor necrosis factor-α (TNF-α) and the rats sacrificed for evaluation of histological changes in their intestine. Results: All groups that were administrated bacteria, whether they were toxin producer or not, showed a decrease in their weights with a reduction of appetite. Serological changes observed included an increase in IL-10 level and an increase in TNF-α level in their sera. Regarding the histological examination, there were noticeable histological changes in the large intestines of all rats given bacterial suspension but not in small intestine. Conclusion: All E.coli isolates which were isolated from IBD patients stool (whether it was microcin B17 producing or not) were able to induce inflammatory responses and histological changes in the intestines of rats . Accordingly, other virulence factors (in addition to Microcin B17) may play role in the pathogenesis of IBD.

Extracellular Vesicles: Novel Potential Therapeutic Agents in Inflammatory Bowel Diseases.

Patients affected by inflammatory bowel diseases (IBD) can nowadays benefit from a growing number of pharmacological options. However, in moderate-to-severe cases, the therapeutic response is still far from optimal, and treatment changes and optimizations are often required. Thus, researchers in this field are strongly engaged in studies aiming to identify new potential therapeutic targets. Extracellular vesicles (EVs) are tiny subcellular bodies with a phospholipid bilayer envelope containing bioactive molecules, which are released from different cells and are involved in intercellular communication. Recent pre-clinical data show their emerging role in the pathogenesis and treatment of IBD. In our review, we summarize current evidence about the function of EVs as active therapeutic agents in ulcerative colitis and Crohn's disease, analyzing the properties of EVs derived from different cellular sources and the mechanisms through which they may improve intestinal inflammation.

Role of autophagy in pathogenesis of ulcerative colitis

Role of autophagy in pathogenesis of ulcerative colitis

Tofacitinib Affects M1-like and M2-like Polarization and Tissue Factor Expression in Macrophages of Healthy Donors and IBD Patients.

Tofacitinib, as inhibitor of Janus kinases (JAK), interrupts the transmission of numerous pro-inflammatory cytokines involved in the pathogenesis of inflammatory bowel diseases (IBD). Therefore, tofacitinib provides a potent option to treat ulcerative colitis (UC). Besides the anti-inflammatory potential, inhibition of widespread JAKs carries the risk of side effects. Macrophages are involved in the form of different subtypes in inflammation, wound healing, and even coagulation. This study aimed to explore the balanced use of tofacitinib in M1-like as well as M2-like macrophages of healthy donors and patients with IBD. Monocytes of healthy donors and patients with chronic courses of IBD were obtained from blood samples. Macrophage colony-stimulating factor (M-CSF)-derived macrophages were treated with tofacitinib (1 µM, 5 µM, 10 µM) and polarized with either lipopolysaccharide and interferon (IFN)-γ towards M1-like-phenotype or with interleukin (IL)-4 towards M2-like-phenotype. ELISA and flow cytometry were used to evaluate cytokine levels and surface molecules. Tofacitinib had a modulating effect on M1-like macrophages whereby the effect on pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-12, IL-23) was less pronounced than the induction of anti-inflammatory IL-10. However, during M2-like polarization tofacitinib impaired the development of the corresponding phenotype becoming evident through decreased IL-10 levels and CD206 expression in treated macrophages. In both phenotypes, tofacitinib strongly downregulated the expression of immunostimulatory molecules (CD80, CD86, CD83, CD40). Furthermore, a dose-dependent correlation between treatment with tofacitinib and expressed tissue factor was noticed. Tofacitinib influences both polarizations (M1/M2) and the expression of tissue factor in a dose-dependent manner.

Hypoxia, hypoxia-inducible factors and inflammatory bowel diseases.

Adequate oxygen supply is essential for maintaining the body's normal physiological function. In chronic inflammatory conditions such as inflammatory bowel disease (IBD), insufficient oxygen reaching the intestine triggers the regulatory system in response to environmental changes. However, the pathogenesis of IBD is still under investigation. Recent research has highlighted the significant role of hypoxia in IBD, particularly the involvement of hypoxia-inducible factors (HIF) and their regulatory mechanisms, making them promising therapeutic targets for IBD. This review will delve into the role of hypoxia, HIF, and the associated hypoxia-inflammatory microenvironment in the context of IBD. Potential interventions for addressing these challenging gastrointestinal inflammatory diseases will also be discussed within this framework.

Selected Cytokines and Metalloproteinases in Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD) is a collective term for two diseases: ulcerative colitis (UC) and Crohn's disease (CD). There are many factors, e.g., genetic, environmental and immunological, that increase the likelihood of these diseases. Indicators of IBDs include extracellular matrix metalloproteinases (MMPs). The aim of this review is to present data on the role of selected cytokines and metalloproteinases in IBD. In recent years, more and more transcriptomic studies are emerging. These studies are improving the characterization of the cytokine microenvironment inside inflamed tissue. It is observed that the levels of several cytokines are consistently increased in inflamed tissue in IBD, both in UC and CD. This review shows that MMPs play a major role in the pathology of inflammatory processes, cancer, and IBD. IBD-associated inflammation is associated with increased expression of MMPs and reduced ability of tissue inhibitors of metalloproteinases (TIMPs) to inhibit their action. In IBD patients in tissues that are inflamed, MMPs are produced in excess and TIMP activity is not sufficient to block MMPs. This review is based on our personal selection of the literature that was retrieved by a selective search in PubMed using the terms "Inflammatory bowel disease" and "pathogenesis of Inflammatory bowel diseases" that includes systematic reviews, meta-analyses, and clinical trials. The involvement of the immune system in the pathophysiology of IBD is reviewed in terms of the role of the cytokines and metalloproteinases involved.

The Effects of Artificial Sweeteners on Intestinal Nutrient-Sensing Receptors: Dr. Jekyll or Mr. Hyde?

The consumption of artificial and low-calorie sweeteners (ASs, LCSs) is an important component of the Western diet. ASs play a role in the pathogenesis of metabolic syndrome, dysbiosis, inflammatory bowel diseases (IBDs), and various inflammatory conditions. Intestinal nutrient-sensing receptors act as a crosstalk between dietary components, the gut microbiota, and the regulation of immune, endocrinological, and neurological responses. This narrative review aimed to summarize the possible effects of ASs and LCSs on intestinal nutrient-sensing receptors and their related functions. Based on the findings of various studies, long-term AS consumption has effects on the gut microbiota and intestinal nutrient-sensing receptors in modulating incretin hormones, antimicrobial peptides, and cytokine secretion. These effects contribute to the regulation of glucose metabolism, ion transport, gut permeability, and inflammation and modulate the gut-brain, and gut-kidney axes. Based on the conflicting findings of several in vitro, in vivo, and randomized and controlled studies, artificial sweeteners may have a role in the pathogenesis of IBDs, functional bowel diseases, metabolic syndrome, and cancers via the modulation of nutrient-sensing receptors. Further studies are needed to explore the exact mechanisms underlying their effects to decide the risk/benefit ratio of sugar intake reduction via AS and LCS consumption.

Current understanding of the aetiology and pathogenesis of inflammatory bowel diseases (Part 1): the role of the immune system, genetic and epigenetic factors

Inflammatory bowel diseases (IBD) have become the subject of numerous scientific studies in clinical practice in recent years. The review is examines in detail key aspects of IBD pathogenesis, including the role of the immune system, stromal components and genetic factors. Particular attention have been paid to the interaction of these factors and influence on the development and course of the disease. The review’s aims to provide a comprehensive understanding of the mechanisms of IBD development and identify potential avenues for diagnosis, therapy and prevention. The main content of the article covers the latest scientific data and clinical observations in the field of gastroenterology, emphasizing the integration of various disciplines in the understanding and treatment of IBD.

Current understanding of the aetiology and pathogenesis of inflammatory bowel diseases (Part 2): the role of the microbiome and nutritional factors

This work reviews current data on the structure of the microbiota and its interaction with the host, and assesses the impact of the microbial community on the immune system and the development of chronic inflammation in the gastrointestinal tract. This review presents current evidence on the influence of diet on the course and therapy of GI tract inflammation. Studies on the role of microbiota and diet in the pathogenesis of ICD have shown that microbial dysbiosis and Epstein-Barr virus can exacerbate the course of ICD. Certain foods worsen symptoms, while a monosaccharide diet favours remission. The results emphasise the importance of an individualised nutritional approach to improve the treatment of IBS.

Multi-omic insight into the molecular networks of mitochondrial dysfunction in the pathogenesis of inflammatory bowel disease

Mitochondrial dysfunction has been linked to the development of inflammatory bowel disease (IBD), but the genetic pathophysiology was not fully elucidated. We employed Mendelian randomization and colocalization analyses to investigate the associations between mitochondrial-related genes and IBD via integrating multi-omics. Summary-level data of mitochondrial gene methylation, expression and protein abundance levels were obtained from corresponding methylation, expression and protein quantitative trait loci studies, respectively. We obtained genetic associations with IBD and its two subtypes from the Inflammatory Bowel Disease Genetics Consortium (discovery), the UK Biobank (replication), and the FinnGen study (replication). We performed summary-data-based Mendelian randomization analysis to assess the associations of mitochondrial gene-related molecular features with IBD. Colocalization analysis was further conducted to assess whether the identified signal pairs shared a causal genetic variant. After integrating the multi-omics data between mQTL-eQTL and eQTL-pQTL, we identified two mitochondrial genes, i.e., PARK7 and ACADM, with tier 1 evidence for their associations with IBD and ulcerative colitis (UC). PDK1 and FISI genes were associated with UC risk with tier 2 and tier 3 evidence, respectively. The methylation of cg05467918 in ACADM was associated with lower expression of ACADM, which fits with the positive effect of cg05467918 methylation on UC risk. Consistently, the inverse associations between gene methylation and gene expression were also observed in PARK7 (cg10385390) and PDK1 (cg17679246), which were corroborated with the protective role in UC. At circulating protein level, genetically predicted higher levels of PARK7 (OR 0.36, 95% CI 0.25-0.52) and HINT1 (OR 0.47, 95% CI 0.30-0.74) were inversely associated with IBD risk; genetically predicted higher level of HINT1 was associated with a decreased risk of Crohn's disease (CD) (OR 0.26, 95% CI 0.14-0.49) and a higher level of ACADM (OR 0.67, 95% CI 0.55-0.83), PDK1 (OR 0.63, 95% CI 0.49-0.81), FIS1 (OR 0.63, 95% CI 0.47-0.83) was associated with a decreased risk of UC. We found that the mitochondrial PARK7 gene was putatively associated with IBD risk, and mitochondrial FIS1, PDK1, and ACADM genes were associated with UC risk with evidence from multi-omics levels. This study identified mitochondrial genes in relation to IBD, which may enhance the understanding of the pathogenic mechanisms of IBD development. XL is supported by the Natural Science Fund for Distinguished Young Scholars of Zhejiang Province (LR22H260001) and Healthy Zhejiang One Million People Cohort (K-20230085).

Differential Manifestations of Inflammatory Bowel Disease Based on Race and Immigration Status

Background and AimsThe prevalence of inflammatory bowel disease (IBD) is increasing globally. In this context, identifying risk factors for severe disease is important. We examined how race/ethnicity and immigration status influence IBD manifestations, treatments, and outcomes in a diverse, tertiary-care safety-net hospital. MethodsWe conducted a single-center retrospective review of all IBD inpatients and outpatients treated from 1997-2017. Using logistic regression modeling, we compared disease onset, treatment, and outcomes by race (White, Black, Hispanic, Asian) and immigration status (US-born vs. foreign-born). ResultsA total of 577 patients were identified, of which 29.8% were White, 27.4% Hispanic, 21.7% Black, and 13.0% Asian. Compared to Whites, Asians were more likely to be male (OR 2.63, 95% CI: 1.45, 5.00), whereas Blacks were more likely to be diagnosed with Crohn’s disease (CD) (OR 1.75, 95% CI: 1.10, 2.77) and more likely to undergo IBD-related intestinal resection (OR 2.49, 95% CI: 1.40, 4.50). Compared to US-born patients, foreign-born patients were more likely to be diagnosed with UC (OR 1.77, 95% CI: 1.04, 3.02). They were also less likely to be diagnosed before 16 years of age (OR 0.19, 95% CI: 0.08, 0.41), to have undergone intestinal resections (OR 0.39, 95% CI: 0.19, 0.83), to have received biologics (OR 0.43, 95% CI: 0.25, 0.76), or to have had dermatologic manifestations (OR 0.12, 95% CI: 0.03, 0.41). ConclusionsIBD phenotype varies by race, although foreign-born patients of all races show evidence of later onset and milder disease. These findings may aid in disease prognostication and clinical management and furthermore may provide insight into intrinsic and environmental influences on IBD pathogenesis.

The Impact of Obesity on Inflammatory Bowel Disease.

Obesity is prevalent in the inflammatory bowel disease (IBD) population, particularly in newly developed countries where both IBD and obesity in the general population are on the rise. The role of obesity in the pathogenesis of IBD was entertained but results from available studies are conflicting. It does, however, appear to negatively influence disease course whilst impacting on our medical and surgical therapies. The pro-inflammatory profile of the visceral adipose tissue might play a role in the pathogenesis and course of Crohn's Disease (CD). Interestingly, isolating the mesentery from the surgical anastomosis using a KONO-S technique significantly decreases anastomotic recurrence rate. Anti-obesity therapy is not widely used in IBD but was suggested as an adjunctive therapy in those patients. In this review, we aimed to highlight the epidemiology of obesity in IBD and to describe its influence on disease course and outcomes.