Factors In Inflammatory Bowel Disease Research Articles

Vascular endothelial growth factor in inflammatory bowel disease: A systematic review and meta-analysis.

Vascular endothelial growth factor (VEGF) is linked to inflammation and angiogenesis, indicating a possible role in inflammatory bowel disease (IBD) and its main clinical manifestations, Crohn's disease (CD) and ulcerative colitis (UC). This systematic review and meta-analysis investigated studies assessing circulating VEGF concentrations in IBD patients and healthy controls, considering the effect of IBD type, sample type and geographical location. A systematic search identified 18 studies (28 group comparators) investigating 1741 IBD patients and 1291 controls. Data were extracted and analysed using standardized mean differences (SMD) with 95% confidence intervals (CI). VEGF concentrations were significantly higher in IBD patients (SMD = .71, 95% CI .38 to 1.04; p < .001). UC patients showed higher VEGF concentrations than CD patients. Serum samples indicated significant VEGF elevations, unlike plasma samples. Significant VEGF increases were observed in studies conducted in Western Europe and Asia, but not in Eastern Europe. No significant differences were found between active and inactive disease. VEGF concentrations are elevated in IBD patients, with variations by disease type, sample type and geography. However, VEGF is not a reliable marker of disease activity. Future research should standardize methods and explore regional influences to enhance VEGF's clinical utility as a biomarker of IBD.

Antibiotic usage within the first year of life has a protective effect against ulcerative colitis in South Korea: A nationwide cohort study

BackgroundAntibiotic usage in early life has been proposed as a risk factor for inflammatory bowel disease, especially Crohn's disease. However, most studies were conducted in Western countries. AimsWe evaluated the association between antibiotic usage and the incidence of inflammatory bowel disease in the Asian population. MethodsThis nationwide population-based retrospective cohort study included 2,941,889 South Korean infants born between 2007 and 2015, using the National Health Insurance Service database. We assessed whether antibiotic use was associated with the incidence of inflammatory bowel disease. Additionally, we conducted sensitivity analyses, considering protopathic bias and dietary variables. The Cox proportional hazards model was used. ResultsAmong 2,941,889 infants, 2,566,390 (87 %) used antibiotics within a year after birth. Antibiotic usage within a year, number of antibiotic classes, and cumulative days of usage were shown to decrease the risk of ulcerative colitis. This association was particularly prominent with earlier antibiotic exposure. Penicillin was the only antibiotic class related to the reduced risk. The results were robust after adjusting for dietary variables and considering protopathic effect. ConclusionsAntibiotic exposure during the first year of life, particularly at a younger age, is linked to a reduced risk of early-onset ulcerative colitis in South Korea.

Early life exposures and risk of inflammatory bowel disease: A nested case-control study in Quebec, Canada

BackgroundEarly life factors for inflammatory bowel disease are likely to impact the gut microbiota. AimWe investigated the associations between early exposures and inflammatory bowel disease. MethodsThis case-control study was nested within the CO·MMUNITY cohort. Cases of Crohn's disease (CD) and ulcerative colitis (UC) were identified using validated algorithms. All cases and randomly selected controls were invited to complete a questionnaire including early life exposures. Analyses were conducted by logistic regression and causal mediation (direct/indirect effects for passive/active smoking). ResultsEarly introduction of solid foods at 3–6 months tended to increase CD risk compared to later introduction (>6 months): OR = 1.23; 95 % CI: 0.96–1.56, but not of UC. Exclusive breastfeeding tended to decrease the risk of CD (OR = 0.77; 95 % CI: 0.55–1.08), less so for UC. Antibiotics tended to decrease CD (OR = 0.89; 95 % CI: 0.74–1.07) and UC (OR = 0.88; 95 % CI: 0.71–1.09). No association was found between pets and CD or UC. Passive smoking increased CD risk (OR = 1.23; 95 % CI: 1.00–1.51), 20 % of which was mediated by active smoking, but not UC. ConclusionDifferences were noticed in early risk factors for CD and UC. The impact of passive smoking was largely independent of active smoking, highlighting its importance for prevention.

Mixed-method Irish study exploring the role of diet in IBD based on an online questionnaire and a patient panel opinion.

Diet is a risk factor in inflammatory bowel diseases (IBD) pathogenesis. This study aims to examine the dietary patterns and beliefs of Irish patients living with IBD through an online questionnaire and subsequent open discussions with an IBD patient collaborator panel (PCP). All data presented here are selected and presented following the PCP's suggestions and views. This mixed-method study included an online questionnaire using a short food frequency questionnaire examining dietary patterns, dietary opinions, beliefs and behaviours (phase I). Six in-person PCP sessions were conducted, where findings from the online questionnaire, diet and lifestyle in the context of IBD were discussed in depth (phase II). The questionnaire revealed that respondents with active IBD are associated with the consumption of high-sugar, processed and meat-based foods while reducing their consumption of high-fibre foods. Individuals with active Crohn's disease have a decrease in overall daily energy consumption and a significant reduction in intake of fibre, non-starch polysaccharides, micronutrients [B vitamins (B1, B2, and B9), vitamin C, calcium] and trace elements (iron, zinc, copper and manganese). The PCP reported that food tolerability is limited during relapse, leading patients to prefer simple carbohydrates for energy, consistent with the dietary intake data. The PCP reported that most dietary advice was received during hospitalisation (relapse), focused on food avoidance, with little follow-up during remission. The consensus among the PCP was that factors, such as disease type, psychological aspects, dietary understanding and support, can influence peoples' dietary choices. In summary, we show that dietary intake in people with IBD varies and may depend on several factors, not just the disease itself. This PCP desires more dietary information and professional support outside of hospitalisation to assist with disease management.

Role of stress and early-life stress in the pathogeny of inflammatory bowel disease.

Numerous preclinical and clinical studies have shown that stress is one of the main environmental factor playing a significant role in the pathogeny and life-course of bowel diseases. However, stressful events that occur early in life, even during the fetal life, leave different traces within the central nervous system, in area involved in stress response and autonomic network but also in emotion, cognition and memory regulation. Early-life stress can disrupt the prefrontal-amygdala circuit thus favoring an imbalance of the autonomic nervous system and the hypothalamic-pituitary adrenal axis, resulting in anxiety-like behaviors. The down regulation of vagus nerve and cholinergic anti-inflammatory pathway favors pro-inflammatory conditions. Recent data suggest that emotional abuse at early life are aggravating risk factors in inflammatory bowel disease. This review aims to unravel the mechanisms that explain the consequences of early life events and stress in the pathophysiology of inflammatory bowel disease and their mental co-morbidities. A review of therapeutic potential will also be covered.

Identification of endoplasmic reticulum stress-associated genes and subtypes for predicting risk signature and depicting immune features in inflammatory bowel disease

Endoplasmic reticulum stress (ERS) becomes a significant factor in inflammatory bowel disease (IBD), like Crohn's disease (CD) and ulcerative colitis (UC). Our research was aimed at identifying molecular markers to enhance our understanding of ERS and inflammation in IBD, recognizing risk factors and high-risk groups at the molecular level, and developing a predictive model on the grounds of based on ERS-associated genes.This research adopted the least absolute shrinkage and selection operator (LASSO) regression and logistic regression to build a predictive model, and categorized IBD patients into high- and low-risk groups, and then identified four gene clusters. Our key findings included a significant increase in drug target gene expression in high-risk groups, notable discrepancies in immune levels, and functions between high-risk and low-risk groups. Notably, the TAP1 gene emerged as a strong predictor with the highest diagnostic value (area under the curve [AUC] = 0.941). TAP1 encodes proteins required for antigenic peptide transfer across the endoplasmic reticulum (ER) membrane, and its potential as a diagnostic marker and therapeutic target is reflected by its overexpression in IBD tissues.Our study established a new ERS-associated gene model which could forecast the risk, immunological status, and treatment efficacy of patients with IBD. These findings suggest potential targets for personalized therapy and highlight the significance of ERS in the etiology and therapy of IBD. Future studies should explore the therapeutic potential of targeting TAP1 and other ERS-related genes for IBD management.

Comparative Risk of Serious Infection With Vedolizumab vs Anti-Tumor Necrosis Factors in Inflammatory Bowel Disease.

Comparative Risk of Serious Infection With Vedolizumab vs Anti-Tumor Necrosis Factors in Inflammatory Bowel Disease.

Comparative Risk of Serious Infection With Vedolizumab vs Anti-Tumor Necrosis Factor in Inflammatory Bowel Disease: Results From Nationwide Swedish Registers.

We aimed to assess the risk of serious infection in patients with inflammatory bowel disease (IBD) treated with vedolizumab compared with those treated with anti-tumor necrosis factors (TNF) and the general population. In this Swedish cohort study, treatment episodes were identified from nationwide health registers. We used Cox regression with propensity score-matched cohorts to estimate hazard ratios (HRs) for incident serious infections, defined as infections requiring hospital admission. During 1,376 treatment episodes in Crohn's disease, the rate of serious infections per 100 person-years (PY) was 5.18 (95% CI = 3.98-6.63) with vedolizumab vs 3.54 (95% CI = 2.50-4.85) with anti-TNF; HR = 1.72 (95% CI = 1.12-2.65), partly explained by more gastrointestinal infections. Compared with the rate of 0.75/100 PY (95% CI = 0.59-0.92) in a matched general population cohort, vedolizumab demonstrated higher risk (HR = 7.00; 95% CI = 5.04-9.72). During 1,294 treatment episodes in ulcerative colitis, the corresponding rates were 3.74/100 PY (95% CI = 2.66-5.11) with vedolizumab vs 3.42/100 PY (95% CI = 2.31-4.89) with anti-TNF; HR = 0.80 (95% CI = 0.47-1.36) during the initial 1.1 years and HR = 2.03 (95% CI = 0.65-6.32) after 1.1 years (truncated due to nonproportional hazards). Pneumonia accounted for 40% of all infections among anti-TNF, whereas no case was observed among vedolizumab episodes. Compared with the rate of 0.69/100 PYs (95% CI = 0.53-0.87) in a matched general population cohort, vedolizumab showed an HR of 5.45 (95% CI = 3.67-8.11). Vedolizumab was associated with increased risks of serious infections compared with anti-TNF in Crohn's disease but not in ulcerative colitis. Nonetheless, the panorama of serious infections seemed to differ between the drugs. Our findings underscore the importance of clinical awareness of infections and the safety profile of the 2 therapies.

Childhood and adolescent residential and farm pesticide exposures and inflammatory bowel disease incidence in a U.S. cohort of women

Background and aimsThere are few known risk factors for inflammatory bowel disease (IBD), an autoimmune disease characterized by chronic intestinal inflammation. Use of specific pesticides has been associated with higher incidence of IBD among pesticide applicators and their spouses, but no study has examined pesticide exposure in early life, a period where the human immune system undergoes rapid changes. We evaluated pesticide use during childhood and adolescence and incidence of IBD among US women enrolled in the Sister Study. MethodsIncident IBD diagnoses between enrollment (2003–2009) and 2021 were identified and validated with medication use and colectomy/colostomy surgery. We estimated hazard ratios (HR) and 95 % confidence intervals (CI) for the relationship of childhood/adolescent residential and farm pesticide exposures with IBD incidence using Cox models, accounting for age, race and ethnicity, education, smoking, and birth year. ResultsWe identified 277 incident IBD cases among 48,382 eligible participants. IBD hazard was elevated among those whose childhood residence was regularly treated with pesticides, especially among those who ever personally applied pesticides (HR = 1.39, 95%CI: 0.65, 2.99). We observed a positive association between IBD and exposure to broadcast pesticide sprays before DDT was banned (>6 times vs. never HR = 1.56, 95%CI: 1.06, 2.31). Among participants who lived on a farm during childhood/adolescence for ≥1 year (N = 9162), IBD hazards were higher among those who were in crop fields during pesticide application (HR = 2.06, 95%CI: 0.94, 4.51) and who ever personally applied pesticides on crops (HR = 1.85, 95%CI: 0.81, 4.18) or livestock (HR = 2.58, 95%CI: 1.14, 5.83). ConclusionEarly-life pesticide exposure may be a novel risk factor for IBD. Practices that reduce pesticide exposure during early life may help reduce the burden of this disease.

Influence of familial forms of inflammatory bowel disease on the use of immunosuppressants, biological agents, and surgery in the era of biological therapies. Results from the ENEIDA project.

Familial inflammatory bowel disease (IBD) history is a controversial prognostic factor in IBD. We aimed to evaluate the impact of a familial history of IBD on the use of medical and surgical treatments in the biological era. Patients included in the prospectively maintained ENEIDA database and diagnosed with IBD after 2005 were included. Familial forms were defined as those cases with at least one first-degree relative diagnosed with IBD. Disease phenotype, the use of biological agents, or surgical treatments were the main outcomes. A total of 5263 patients [2627 Crohn's disease (CD); 2636 ulcerative colitis (UC)] were included, with a median follow-up of 31months. Of these, 507 (10%) corresponded to familial forms. No clinical differences were observed between familial and sporadic IBD forms except a lower age at IBD diagnosis and a higher rate of males in familial forms of UC. In CD, the proportions of patients treated with thiopurines (54.4% vs 46.7%; P = .015) and survival time free of thiopurines (P = .009) were lower in familial forms. No differences were found regarding the use of biological agents. Concerning surgery, a higher rate of intestinal resections was observed in sporadic CD (14.8% vs 9.9%, P = .027). No differences were observed in UC. In the era of biological therapies, familial and sporadic forms of IBD show similar phenotypes and are managed medically in a similar way; whether these is due to lack of phenotypical differences or an effect of biological therapies is uncertain. What is already known on this topic: IBD's etiopathogenesis points to an interaction between environmental and genetic factors, being familial history a controversial prognostic factor. Biological agents use and need for surgery regarding familial or sporadic forms of IBDs present conflicting results. What this study adds: Familial and sporadic forms of IBD have similar phenotypes and are managed medically and surgically in a similar way. How this study might affect research, practice or policy: Familial aggregation should not be considered a factor associated with more aggressive disease.

Umbrella review of risk factors for inflammatory bowel disease: a study protocol

IntroductionInflammatory bowel disease (IBD) is a chronic idiopathic inflammatory disorder that arises from complex interactions between genetics, environment and gut microbiota. It encompasses Crohn’s disease, ulcerative colitis and IBD-unclassified. The...

Pregnancy period and early-life risk factors for inflammatory bowel disease: a Northern Finland birth cohort 1966 study

BackgroundThe pathogenesis of inflammatory bowel disease (IBD) has not been fully elucidated. The aim of this study was to analyze the pregnancy period, perinatal period, and infancy period risk factors for IBD in a well-characterized birth cohort from Northern Finland.MethodsThe Northern Finland Birth Cohort 1966 (NFBC1966) population comprises mothers living in the two northernmost provinces of Finland, Oulu, and Lapland, with dates of delivery between Jan 1st and Dec 31st, 1966 (12 055 mothers, 12 058 live-born children, 96.3% of all births during 1966). IBD patients were identified using hospital registries (from 1966 to 2020) and Social Insurance Institution (SII) registry reimbursement data for IBD drugs (from 1978 to 2016). The data were analyzed by Fisher’s exact test and logistic regression.ResultsIn total, 6972 individuals provided informed consent for the use of combined SII and hospital registry data. Of those, 154 (2.1%) had IBD (113 [1.6%] had ulcerative colitis (UC), and 41 (0.6%) had Crohn’s disease (CD)). According to multivariate analysis, maternal smoking > 10 cigarettes/day during pregnancy was associated with a nearly 6-fold increased risk of CD in the offspring (OR 5.78, 95% CI 1.70–17.3). Breastfeeding (OR = 0.18, 95% CI 0.08–0.44) and iron supplementation during the first year of life (OR = 0.43, 95% CI 0.21–0.89) were negatively associated with CD.ConclusionsSmoking during pregnancy was associated with the risk of CD while Breastfeeding and oral iron supplementation at infancy were negatively associated with the risk of CD later in life.

Crohn’s disease in patients with Hirschsprung disease and Hirschsprung-associated enterocolitis: A review

In the last decade, the incidence of inflammatory bowel disease in children has been increasing. Some studies have reported the development of Crohn’s disease in patients with Hirschsprung disease and Hirschsprung-associated enterocolitis. Suggestions have been made about the possible causes of the development of Crohn’s-like lesions after intestinal resection in early childhood. This study aimed to summarize information about Hirschsprung-associated Crohn’s disease and Crohn’s-like lesions after surgical treatment of Hirschsprung disease. The search was carried out in scientific databases of eLibrary, PubMed, ScienceDirect, and Google Scholar. The search time interval was 2000–2023. Fourteen articles dedicated to Hirschsprung-associated Crohn’s disease were identified. Common pathogenesis factors in inflammatory bowel diseases and Hirschsprung-associated enterocolitis were identified, such as microbiota disturbance and chronic inflammation. Predisposing factors for pathological immune response to dysbiosis and incidence of enterocolitis included enteric nervous system dysfunction, impaired neuroimmune regulatory mechanisms, general immunological disturbance, and “immaturity” and abnormality of the barrier function of the intestinal mucosa. The “classic form” of Crohn’s disease may not develop in patients with Hirschsprung disease and recurrent attacks of enterocolitis but Crohn’s-like lesions. Persistent functional or organic obstruction after surgical treatment of Hirschsprung disease enhances the negative effect of predisposing factors, leading to chronic inflammation of the intestinal mucosa. Delayed occurrence of Hirschsprung-associated enterocolitis is a predisposing factor for the development of chronic inflammation. When Hirschsprung-associated enterocolitis occurs repeatedly, endoscopic assessment should be performed for the exclusion of Crohn’s disease and chronic inflammatory changes in the anastomosis area for treatment selection.

DHX9 maintains epithelial homeostasis by restraining R-loop-mediated genomic instability in intestinal stem cells

Epithelial barrier dysfunction and crypt destruction are hallmarks of inflammatory bowel disease (IBD). Intestinal stem cells (ISCs) residing in the crypts play a crucial role in the continuous self-renewal and rapid recovery of intestinal epithelial cells (IECs). However, how ISCs are dysregulated in IBD remains poorly understood. Here, we observe reduced DHX9 protein levels in IBD patients, and mice with conditional DHX9 depletion in the intestinal epithelium (Dhx9ΔIEC) exhibit an increased susceptibility to experimental colitis. Notably, Dhx9ΔIEC mice display a significant reduction in the numbers of ISCs and Paneth cells. Further investigation using ISC-specific or Paneth cell-specific Dhx9-deficient mice demonstrates the involvement of ISC-expressed DHX9 in maintaining epithelial homeostasis. Mechanistically, DHX9 deficiency leads to abnormal R-loop accumulation, resulting in genomic instability and the cGAS-STING-mediated inflammatory response, which together impair ISC function and contribute to the pathogenesis of IBD. Collectively, our findings highlight R-loop-mediated genomic instability in ISCs as a risk factor in IBD.

Accumulated LPS induced by colitis altered the activities of vitamin D-metabolizing hydroxylases and decreased the generation of 25-hydroxyvitamin D

It is generally accepted that low vitamin D (VD) levels are associated with a high prevalence factor for Inflammatory bowel disease (IBD). IBD patients have observed higher levels of lipopolysaccharide (LPS), ALT, and AST than healthy people. Gut-derived LPS causes inflammatory injury in the liver and kidney. The VD-metabolizing mechanism is involved in the liver and kidney, which means IBD might impact VD metabolism. However, whether IBD affects VD metabolism has not been studied. In vitro LPS resulted in decreased CYP2R1 in liver cells as well as decreased CYP27B1 and increased CYP24A1 in kidney cells, revealing that LPS changed the activities of several hydroxylases. Mice with acute colitis had an increased LPS in serum and liver with mild hepatic injuries, while mice with chronic colitis had a significant elevation of LPS in serum, liver, and kidney with hepatorenal injuries. Thus, the liver hydroxylase for VD metabolism would be the first to be affected in IBD. Consequently, serum 25-hydroxyvitamin D declined dramatically with a significant elevation of 24,25-dihydroxyvitamin D and 1,24,25-trihydroxyvitamin D. Unchanged serum levels of 1,25-dihydroxyvitamin D might be the result of other factors in vivo. In acute colitis, a small dosage (4 IU/day) of cholecalciferol could protect the colon, decrease the serum level of LPS, and finally increase serum 25-hydroxyvitamin D. However, this improvement of cholecalciferol was fading in chronic colitis. These results suggested that VD supplementations for preventing and curing IBD in the clinic should consider hepatorenal hydroxylases and be employed as soon as possible for a better outcome.

Increased bronchiectasis risk and related risk factors in inflammatory bowel disease: a 10-year Korean national cohort study.

The association between inflammatory bowel disease (IBD) and an increased risk of bronchiectasis, as well as contributing factors, remains unclear. Additionally, whether bronchiectasis increases disease burden in IBD remains unknown. Therefore, this study aimed to: 1) assess whether IBD increases the risk of incident bronchiectasis; 2) compare the risk of bronchiectasis between individuals with Crohn's disease (CD) and those with ulcerative colitis (UC); 3) identify risk factors for bronchiectasis in individuals with IBD; and 4) examine the disease burden in individuals with IBD and bronchiectasis versus those without. We conducted a population-based matched cohort study involving adults aged ≥20 years with IBD, using data acquired from the Korean National Health Insurance Service-National Sample Cohort database between 2002 and 2012. During the mean follow-up of 9.6 years, the incidence rate of bronchiectasis was 419.63 out of 100 000 person-years (PY) and 309.65 out of 100 000 PY in the IBD and matched cohorts (adjusted hazard ratio (aHR) 1.21, 95% CI 1.05-1.39), respectively. UC was associated with increased bronchiectasis risk (aHR 1.42, 95% CI 1.19-1.69), but CD was not. Multivariate Cox regression analyses showed that age, male sex, medical aid, underweight status, COPD and diabetes mellitus were associated with an increased risk of bronchiectasis in the IBD cohort (p<0.05). The mortality, emergency department visit and hospitalisation rates were significantly higher for individuals with IBD and bronchiectasis compared with those without bronchiectasis (p<0.05). IBD is associated with increased risk of bronchiectasis, which results in a greater disease burden in individuals with IBD.

Integrated 16S rRNA sequencing and metagenomics insights into microbial dysbiosis and distinct virulence factors in inflammatory bowel disease.

The escalation of urbanization correlates with rising rates of inflammatory bowel disease (IBD), necessitating research into new etiological factors. This study aims to elucidate the gut microbiota profiles in IBD patients and compare them with healthy controls in a western city of China. We conducted a multicenter case-control study from the end of 2020, using 16S rRNA gene sequencing (n = 36) and metagenomic sequencing (n = 12) to analyze the gut microbiota of newly diagnosed IBD patients, including those with Crohn's disease (CD) and ulcerative colitis (UC). Our results demonstrated a significant enrichment of the phylum Proteobacteria, particularly the genus Escherichia-Shigella, in CD patients. Conversely, the genus Enterococcus was markedly increased in UC patients. The core gut microbiota, such as the Christensenellaceae R-7 group, Fusicatenibacter, and Holdemanella, were primarily identified in healthy subjects. Additionally, significant interactions between the microbiome and virulence factors were observed. The findings suggest that oxidative stress may play a pivotal role in the pathology of IBD. This study contributes to the growing dialogue about the impact of gut microbiota on the development of IBD and its variations across different geographies, highlighting potential avenues for further research.

Human-derived bacterial strains mitigate colitis via modulating gut microbiota and repairing intestinal barrier function in mice

BackgroundUnbalanced gut microbiota is considered as a pivotal etiological factor in colitis. Nevertheless, the precise influence of the endogenous gut microbiota composition on the therapeutic efficacy of probiotics in colitis remains largely unexplored.ResultsIn this study, we isolated bacteria from fecal samples of a healthy donor and a patient with ulcerative colitis in remission. Subsequently, we identified three bacterial strains that exhibited a notable ability to ameliorate dextran sulfate sodium (DSS)-induced colitis, as evidenced by increased colon length, reduced disease activity index, and improved histological score. Further analysis revealed that each of Pediococcus acidilactici CGMCC NO.17,943, Enterococcus faecium CGMCC NO.17,944 and Escherichia coli CGMCC NO.17,945 significantly attenuated inflammatory responses and restored gut barrier dysfunction in mice. Mechanistically, bacterial 16S rRNA gene sequencing indicated that these three strains partially restored the overall structure of the gut microbiota disrupted by DSS. Specially, they promoted the growth of Faecalibaculum and Lactobacillus murinus, which were positively correlated with gut barrier function, while suppressing Odoribacter, Rikenella, Oscillibacter and Parasutterella, which were related to inflammation. Additionally, these strains modulated the composition of short chain fatty acids (SCFAs) in the cecal content, leading to an increase in acetate and a decrease in butyrate. Furthermore, the expression of metabolites related receptors, such as receptor G Protein-coupled receptor (GPR) 43, were also affected. Notably, the depletion of endogenous gut microbiota using broad-spectrum antibiotics completely abrogated these protective effects.ConclusionsOur findings suggest that selected human-derived bacterial strains alleviate experimental colitis and intestinal barrier dysfunction through mediating resident gut microbiota and their metabolites in mice. This study provides valuable insights into the potential therapeutic application of probiotics in the treatment of colitis.

ERCC4: a potential regulatory factor in inflammatory bowel disease and inflammation-associated colorectal cancer.

The pathogenesis of inflammatory bowel disease (IBD) remains unclear and is associated with an increased risk of developing colitis-associated cancer (CAC). Under sustained inflammatory stimulation in the intestines, loss of early DNA damage response genes can lead to tumor formation. Many proteins are involved in the pathways of DNA damage response and play critical roles in protecting genes from various potential damages that DNA may undergo. ERCC4 is a structure-specific endonuclease that participates in the nucleotide excision repair (NER) pathway. The catalytic site of ERCC4 determines the activity of NER and is an indispensable gene in the NER pathway. ERCC4 may be involved in the imbalanced process of DNA damage and repair in IBD-related inflammation and CAC. This article primarily reviews the function of ERCC4 in the DNA repair pathway and discusses its potential role in the processes of IBD-related inflammation and carcinogenesis. Finally, we explore how this knowledge may open novel avenues for the treatment of IBD and IBD-related cancer.

The role of granulocyte-macrophage colony-stimulating growth factor in inflammatory bowel diseases

Inflammatory bowel diseases, which include ulcerative colitis and Crohn's disease, are chronic immune-inflammatory diseases of the intestine that are increasing in prevalence and incidence worldwide. They are progressive, with the need for lifelong therapy, a high risk of surgical interventions and a decrease in the quality of life of patients. The results of clinical and population studies indicate that the possibilities of modern therapy for inflammatory bowel diseases have reached their maximum. Its effectiveness in achieving complete clinical and endoscopic remission, despite the use of genetically engineered biological drugs, is estimated at 35-40%, which is obviously insufficient. A possible solution to this problem could be the inclusion of granulocyte-macrophage colony-stimulating factors in treatment regimens for inflammatory bowel diseases in combination with glucocorticosteroids, cytostatics and biological therapy drugs. A review of a number of experimental and clinical studies that confirmed the clinical effectiveness of macrophage growth factors is the subject of this article.