Microbiota In Inflammatory Bowel Disease Research Articles

From gut to brain: understanding the role of microbiota in inflammatory bowel disease.

With the proposal of the "biological-psychological-social" model, clinical decision-makers and researchers have paid more attention to the bidirectional interactive effects between psychological factors and diseases. The brain-gut-microbiota axis, as an important pathway for communication between the brain and the gut, plays an important role in the occurrence and development of inflammatory bowel disease. This article reviews the mechanism by which psychological disorders mediate inflammatory bowel disease by affecting the brain-gut-microbiota axis. Research progress on inflammatory bowel disease causing "comorbidities of mind and body" through the microbiota-gut-brain axis is also described. In addition, to meet the needs of individualized treatment, this article describes some nontraditional and easily overlooked treatment strategies that have led to new ideas for "psychosomatic treatment".

A42 A HIGH SALT DIET INCREASES ELASTOLYTIC ACTIVITY AND WORSENS COLITIS IN GNOTOBIOTIC MICE

Abstract Background Recent evidence has linked ultra-processed foods, which are high in salt, to increased risk of inflammatory bowel disease (IBD). A high salt diet (HSD) was also shown to be colitogenic in specific pathogen-free mice, in part, through modulation of the microbiota. We recently described high microbial proteolytic activity (PA) in feces from IBD patients, that when transferred to germ-free mice, increased acute colitis severity. However, the drivers of high microbial PA are unknown. Aims To determine whether HSD increases proteolytic activity, thereby exacerbating colitis. Methods Adult germ-free (GF) C57BL/6 mice were colonized with feces from a patient with UC in flare (n=13). Mice were fed either a control diet (CD; 7004, Teklad) or a HSD (7004 supplemented with 4% NaCl) plus 1% NaCl in drinking water. Three weeks following colonization, chronic colitis was induced in half of the mice by three cycles (five days each; 2.0%, 1.5% and 1.5%, respectively) of DSS in drinking water with a five-day wash-out period between cycles. Fecal PA and predicted microbial protease profiles were measured before colitis induction. Weight loss and disease activity (e.g., occult blood in feces and stool consistency) was evaluated for the duration of colitis and microscopic colitis was evaluated at endpoint. Results In mice colonized with UC microbiota, a HSD increased elastolytic activity (p=.03 versus CD) and induced a unique predicted protease and peptidase profile. After colitis induction, mice consuming a HSD lost more weight than mice consuming the CD (p=.0001) and had higher disease activity (p=.0004). Additionally, HSD induced more severe microscopic colitis scores compared with the CD (p=.0001). Conclusions These results raise the hypothesis that a HSD drives microbial proteolytic activity of IBD microbiota. However, whether this shift is causally associated with the worsening of colitis remains unclear. Mechanistic insight underlying this HSD-microbial proteolytic function could lead to specific dietary modifications or anti-proteolytic therapies for IBD in patients with proteolytic-driven inflammation. Funding Agencies CCC, CIHR

P1214 The crosstalk between oral and intestinal microbiota in inflammatory bowel disease patients

Abstract Background Background: Previous studies reported that oral microbes can migrate to the gut, but the relationship between oral and intestinal microbiota in inflammatory bowel disease (IBD) is still unclear. Methods Here, we investigated the oral and gut microbiota of patients with Crohn’s disease (CD) and ulcerative colitis (UC), as well as their healthy relatives. We combined second- and third-generation sequencing based on the 16S rRNA gene to analyze the oral and fecal microbiota. Results A total of 97 IBD patients (59 CD and 38 UC) and 94 healthy relatives were included in the study. Our finding showed that CD and UC patients had higher levels of pathogenic bacteria in both their oral and fecal microbiota. In IBD patients, the gut microbiome was more influenced by the oral microbiome compared to healthy relatives, particularly in CD. We also observed an interesting interaction between Veillonella and Escherichia-Shigella in CD, and the presence of Veillonella in the gut was associated with disease activity. We developed diagnostic models that combined oral and fecal genera, which effectively distinguished CD (AUC=0.8478) and UC (AUC=0.7826) from healthy relatives, as well as predicted active inflammation in CD (AUC=0.9226) and UC (AUC=0.9158). Additionally, our third-generation sequencing results revealed an increase in Parvimonas micra in the oral cavity of IBD patients, and this was positively correlated with its presence in the feces. Conclusion These findings suggest that both oral and gut microbiota may play a crucial role in the development of IBD and could be potential targets for intervention.

Nutritional modulation of gut microbiota in inflammatory bowel disease: a systematic review

Introduction: Inflammatory bowel diseases (IBD) have shown an increase in incidence worldwide. The pathogenesis of IBD is that genetically susceptible individuals develop intolerance to dysregulated gut microbiota (dysbiosis) and chronic inflammation develops as a result of poor dietary triggers. Diet plays an important role in modulating the gut microbiota and can be applied as a therapeutic tool to improve the course of the disease. Objective: It was to carry out a systematic review of the main interactions between nutrology, gut microbiota, and inflammatory bowel disease, to elucidate the main clinical outcomes of the disease after nutrological treatment, analyzing the main macro and micronutrients. Methods: The PRISMA Platform systematic review rules were followed. The search was carried out from August to October 2023 in the Scopus, PubMed, Science Direct, Scielo, and Google Scholar databases. The quality of the studies was based on the GRADE instrument and the risk of bias was analyzed according to the Cochrane instrument. Results and Conclusion: 144 articles were found. A total of 39 articles were evaluated in full and 30 were included and developed in the present systematic review study. Considering the Cochrane tool for risk of bias, the overall assessment resulted in 27 studies with a high risk of bias and 22 studies that did not meet GRADE and AMSTAR-2. Most studies showed homogeneity in their results, with X2=59.9%>50%. With nutritional treatment, several micronutrients have the potential to modulate intestinal inflammation. Immunonutrition has demonstrated its importance through vitamins A, C, E, and D, folic acid, beta-carotene, and trace elements such as zinc, selenium, manganese, and iron. The Specific Carbohydrate Diet, fermentable oligosaccharides, disaccharides, monosaccharides, and polyol diet, and the Mediterranean diet also appear to show strong anti-inflammatory properties and promise to improve symptoms of inflammatory bowel disease. Diet modulation can control IBD by reducing persistent intestinal symptoms, balancing the gut microbiota, and reducing markers of inflammation. Dietary therapy can improve the quality of life of IBD patients.

The Impact of Dietary Interventions on the Microbiota in Inflammatory Bowel Disease: A Systematic Review

Abstract Background and Aims Diet plays an integral role in the modulation of the intestinal environment, with the potential to be modified for management of individuals with inflammatory bowel disease [IBD]. It has been hypothesised that poor ‘Western-style’ dietary patterns select for a microbiota that drives IBD inflammation and, that through dietary intervention, a healthy microbiota may be restored. This study aimed to systematically review the literature and assess current available evidence regarding the influence of diet on the intestinal microbiota composition in IBD patients, and how this may affect disease activity. Methods MEDLINE, EMBASE, Scopus, Web of Science, and Cochrane Library were searched from January 2013 to June 2023, to identify studies investigating diet and microbiota in IBD. Results Thirteen primary studies met the inclusion criteria and were selected for narrative synthesis. Reported associations between diet and microbiota in IBD were conflicting due to the considerable degree of heterogeneity between studies. Nine intervention studies trialled specific diets and did not demonstrate significant shifts in the diversity and abundance of intestinal microbial communities or improvement in disease outcomes. The remaining four cross-sectional studies did not find a specific microbial signature associated with habitual dietary patterns in IBD patients. Conclusions Diet modulates the gut microbiota, and this may have implications for IBD; however, the body of evidence does not currently support clear dietary patterns or food constituents that are associated with a specific microbiota profile or disease marker in IBD patients. Further research is required with a focus on robust and consistent methodology to achieve improved identification of associations.

Fatty acids and lipid mediators in inflammatory bowel disease: from mechanism to treatment.

Inflammatory Bowel Disease (IBD) is a chronic, relapsing inflammatory disorder of the gastrointestinal tract. Though the pathogenesis of IBD remains unclear, diet is increasingly recognized as a pivotal factor influencing its onset and progression. Fatty acids, essential components of dietary lipids, play diverse roles in IBD, ranging from anti-inflammatory and immune-regulatory functions to gut-microbiota modulation and barrier maintenance. Short-chain fatty acids (SCFAs), products of indigestible dietary fiber fermentation by gut microbiota, have strong anti-inflammatory properties and are seen as key protective factors against IBD. Among long-chain fatty acids, saturated fatty acids, trans fatty acids, and ω-6 polyunsaturated fatty acids exhibit pro-inflammatory effects, while oleic acid and ω-3 polyunsaturated fatty acids display anti-inflammatory actions. Lipid mediators derived from polyunsaturated fatty acids serve as bioactive molecules, influencing immune cell functions and offering both pro-inflammatory and anti-inflammatory benefits. Recent research has also highlighted the potential of medium- and very long-chain fatty acids in modulating inflammation, mucosal barriers, and gut microbiota in IBD. Given these insights, dietary intervention and supplementation with short-chain fatty acids are emerging as potential therapeutic strategies for IBD. This review elucidates the impact of various fatty acids and lipid mediators on IBD and delves into potential therapeutic avenues stemming from these compounds.

Preparing xylooligosaccharides from paper mulberry branches as a promising prebiotic candidate for in vitro regulation of intestinal microbiota in colitis

Xylooligosaccharides riched in xylobiose and xylotriose exhibit various biological activities as prebiotics. However, the prebiotics of xylooligosaccharides for regulating the intestinal microbiota in colitis models has been rarely investigated. In this study, differences in prebiotic ability of xylooligosaccharides samples from paper mulberry branches using different methods, including autohydrolysis (termed as 170AH), sequent purification by polystyrene-divinylbenzene copolymer resin (termed as 170AH-XAD), and enzymatic hydrolysis using endo-β-1,4-xylanase (170AH-XAD-E) were investigated. Results revealed that 170AH-XAD-E possessing higher fractions of xylobiose and xylotriose exhibited the best performance in vitro by promoting the proliferation of Bifidobacterium adolescentis and Lactobacillus acidophilus, with utilization rates of 92.30% and 91.00%, respectively. Additionally, 170AH-XAD-E outperformed the other samples in increasing the species' abundance of in vivo intestinal microbiota in colitis mouse model induced by Escherichia coli. Furthermore, 170AH-XAD-E selectively promoted the growth of Bacteroides, while inhibiting the proliferation of Firmicutes, Proteobacteria, and Actinobacteriota. These abilities of 170AH-XAD-E may be due to its potential to upregulate the population of intestinal microbiota associated with the functional abundance of Cell wall/membrane/envelope biogenesis and Inorganic ion transport and metabolism. Overall, this work demonstrates that XOS with high contents of xylobiose and xylotriose possesses excellent potential as intestinal microbiota regulators and anti-colitis agents.

The Intertwining Roads between Psychological Distress and Gut Microbiota in Inflammatory Bowel Disease.

Inflammatory bowel disease represents one of the most life-altering gastrointestinal pathologies, with its multifactorial nature and unclear physiopathology. The most relevant clinical forms, ulcerative colitis and Crohn's disease, clinically manifest with mild to severe flares and remission periods that alter the patient's social, familial and professional integration. The chronic inflammatory activity of the intestinal wall determines severe modifications of the local environment, such as dysbiosis, enteric endocrine, nervous and immune system disruptions and intestinal wall permeability changes. These features are part of the gastrointestinal ecosystem that modulates the bottom-to-top signaling to the central nervous system, leading to a neurobiologic imbalance and clinical affective and/or behavioral symptoms. The gut-brain link is a bidirectional pathway and psychological distress can also affect the central nervous system, which will alter the top-to-bottom regulation, leading to possible functional digestive symptoms and local inflammatory responses. In the middle of this neuro-gastrointestinal system, the microbiome is a key player, as its activities offer basic functional support for both relays. The present article presents current scientific information that links the pathophysiology and clinical aspects of inflammatory bowel disease and psychiatric symptomatology through the complex mechanism of the gut-brain axis and the modulatory effects of the gut microbiota.

The Protective Role of TLR4 in Intestinal Epithelial Cells through the Regulation of the Gut Microbiota in DSS-Induced Colitis in Mice.

The cause of ulcerative colitis (UC) is not yet fully understood. Previous research has pointed towards a potential role for mutations in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) in promoting the onset and progression of inflammatory bowel disease (IBD) by altering the microbiota of the gut. However, the relationship between toll-like receptor 4 (TLR4) and gut microbiota in IBD is not well understood. To shed light on this, the interaction between TLR4 and gut microbiota was studied using a mouse model of IBD. To examine the function of TLR4 signaling in intestinal injury repair, researchers developed Dextran Sulfate Sodium Salt (DSS)-induced colitis and injury models in both wild-type (WT) mice and TLR4 knockout (TLR4-KO) mice. To assess changes in the gut microbiota, 16S rRNA sequencing was conducted on fecal samples from both the TLR4-KO and WT enteritis mouse models. The data obtained depicted a protective function of TLR4 against DSS-induced colitis. The gut microbiota composition was found to vary considerably between the WT and TLR4-KO mice groups as indicated by β-diversity analysis and operational taxonomic units (OTUs) cluster. Statistical analysis of microbial multivariate variables depicted an elevated abundance of Escherichia coli/Shigella, Gammaproteobacteria, Tenerlcutes, Deferribacteres, Enterobacteria, Rikenellaceae, and Proteobacteria in the gut microbiota of TLR4-KO mice, whereas there was a considerable reduction in Bacteroidetes at five different levels of the phylogenetic hierarchy including phylum, class, order, family, and genus in comparison with the WT control. TLR4 may protect intestinal epithelial cells from damage in response to DSS-induced injury by controlling the microbiota in the gut.

Effect of gut microbiome alteration in inflammatory bowel disease

High morbidity rates are associated with inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. New studies have suggested that dysbiosis may play a role in the etiology of inflammatory bowel disease, although the cause of IBD remains unknown. Several disease pathologies, such as inflammatory bowel disease, have been associated with the intestinal microbiota, a metabolic organ with multiple physiological functions. This review summarizes the present level of knowledge regarding the impact of altered gut microbiota in inflammatory bowel disease, the mechanisms by which this occurs, and the potential significance of therapeutic methods based on gut microbiota in the prevention and treatment of IBD. It has been demonstrated that directly targeting the intestinal microbiota can treat both inflammatory bowel disease and colitis in humans and animals. To characterize the core microbiome associated with IBD and the underlying pathophysiology, however, additional research employing well-designed randomized control trials and animal models is required, as there are currently insufficient data and contradictory results from previous studies. The environment will influence the probiotic and prebiotic treatment for IBD.

Effects of hydroxychloroquine on intestinal mucosal barrier and gut microbiota in inflammatory-bowel disease of mice

Hydroxychloroquine (HCQ) effect on gut microbiota and intestinal mucosal barrier in Inflammatory-Bowel Disease (IBD) was evaluated in this work. Here, we established an IBD model before treating mice with HCQ. After HCQ treatment, the body weight, colon length and fecal occult blood of mice did not change significantly.

Evidence from clinical studies of the nutrological modulation of the gut microbiota in inflammatory bowel diseases: a systematic review

Introduction: The main risk factor for inflammatory bowel disease (IBD) is a positive family history in 10-25% of patients. Crohn's disease (CD) can affect individuals from 15 to 40 years old and from 50 to 80 years old, more frequently in women. Ulcerative colitis (UC) can start at any age. The pathogenesis of IBD is linked to genetically susceptible individuals, dysregulated gut microbiota (dysbiosis), chronic inflammation, and poor dietary patterns. Diet plays an important role in modulating the gut microbiota and can be applied as a therapeutic tool to improve the course of the disease. Objective: To carry out a systematic review of the main interactions between dietary therapy, gut microbiota, and inflammatory bowel disease, to elucidate the main clinical outcomes after nutrological treatment. Methods: The present study followed the international model of systematic review (PRISMA). Clinical studies were included, involving randomized controlled, prospective, and retrospective studies published from 2010 to 2022. Results: It was founded 87 studies on diet modulation in the control of IBD. These studies showed reductions in persistent intestinal symptoms, improvement of gut microbiota, reduction of inflammation markers, and improvement in quality of life, with p<0.05 (95% CI). The studies were homogeneous (X2 = 98.9%), which increases the reliability of the clinical results on the dietary importance in the modulation of IBD. Conclusion: The important role of diet modulation in the control and even in the remission of IBD was evidenced.

P912 Increased Primary Bile Acids with Ileocolonic Resection Impact Ileal Inflammation and Gut Microbiota in Inflammatory Bowel Disease

Abstract Background A majority of Crohn’s disease (CD) patients require surgery. Ileitis recurs after most ileocolectomies and is a critical determinant for outcomes. The impact of ileocolectomy-induced bile acid (BA) perturbations on intestinal microbiota and inflammation are unknown. We characterized relationships between ileocolectomy, stool BA, microbiota, and intestinal inflammation in inflammatory bowel disease (IBD). Methods Validated IBD clinical and endoscopic assessments were prospectively collected. Matched primary and secondary BA concentrations measured in stool using Agilent Quadrupole Time of Flight Liquid chromatography-mass spectrometry were compared based on ileocolectomy and ileitis status. Primary BA thresholds for ileitis were evaluated using area under the receiver operating characteristic curve analyses. In CD, endoscopic remission was defined as SES-CD <3 or Rutgeerts <i2b. Ileal ER was defined as ileal SES-CD ≤ 1 and colonic ER was defined as colonic SES-CD≤2 without any segment >1. In UC, ER was defined as UC-ESS ≤ 1. Metagenomic sequencing profiled microbial composition and function. Relationships between ileocolectomy, BA and microbiota were assessed. Results In 166 patients, elevated primary and secondary BA existed with ileocolectomy. With ileitis, only primary BA (795 nMol/g vs 398 nMol/g, p=0.009) were higher compared to without ileitis. The optimal primary BA threshold (≥228nMol/g) identified ileitis on multivariable analysis (OR=2.3, p=0.04). Similar primary (471 nMol/g vs. 606 nMol/g, p=0.8) and secondary (382 nMol/g vs. 242 nMol/g, p=0.2) BA concentrations existed with and without colonic inflammation. Microbial diversity (Shannon index, p=0.0006), Faecalibacterium prausnitzii and O-acetylhomoserine aminocarboxypropyltransferase (MetY, p=0.0002) were decreased with elevated primary BA. Amongst ileocolectomy patients, only those with elevated primary BA had diversity (p=0.01), F.prausnitzii and MetY (p=0.04) reductions. Those with both ileocolectomy and intermediate (p=0.002) or high (≥228nMol/g, p=9.1e-11) ) primary BA had reduced F.prausnitzii compared to without ileocolectomy (Figure 1). Those with ileocolectomy and low (<29.2nMol/g) primary BA had similar F.prausnitzii as those without ileocolectomy (P=0.13). MetY was reduced with ileitis (p=0.02). Conclusion Elevated primary bile acids were associated with ileitis, and reduced microbial diversity, F.prausnitzii abundance, and enzymatic expression of MetY (acetate and L-methionine producing enzyme expressed by F.prausnitzii) and were the only factor associated with these findings after ileocolectomy.

DOP50 Impact of Inflammatory Bowel Disease associated dysbiosis on bacterial quorum sensing mediated by Acyl-homoserine Lactone in human gut microbiota

Abstract Background Intestinal dysbiosis is a key feature in the pathogenesis of inflammatory bowel diseases (IBD). Bacterial quorum sensing mediated by acyl-homoserine lactones (AHL) might play a role in the dialogue between the gut microbiota and the host. The main objective of our study was to investigate the presence and expression of AHL synthase and receptor genes in the human gut ecosystem during IBD. Methods To confirm the presence of AHL in the gut, mass spectrometric detection was performed on stool samples from IBD patients and non-IBD subjects. Then, by an in silico approach, we exploited the open access database: Inflammatory Bowel Disease Multi’omics Database, an American cohort with bacterial metagenomes and metatranscriptomes data of stool samples from non-IBD and IBD subjects. To characterise gut dysbiosis, the most discriminating bacterial species between non-IBD and IBD patients were identified by multivariate analysis and allowed us to define two groups (dysbiosis/non-dysbiosis). The search for AHL synthase (luxI) and receptor (luxR) known homolog genes, was performed using Basic Local Alignment Search Tool (BLAST) from previously assembled gene files (presence/absence) as well as raw data sequencing files (relative abundance and expression). Results Mass spectrometry confirmed a higher concentration of AHL molecules in healthy subjects than in relapsing IBD. Regarding in silico analysis, 103 subjects were selected including 50 with Crohn’s disease (CD), 27 with ulcerative colitis (UC), and 26 non-IBD subjects. No luxI-like synthase genes were retrieved by BLAST searches. However, several homologs of receptor genes were identified: sdiA gene from Escherichia coli (7/103 patients) and luxR-like homologs from Bacteroides fragilis and Bacteroides dorei present in all patients. According to disease, only one luxR-like gene from Bacteroides dorei was under-expressed in IBD patients (p = 0.02) compared to non-IBD, especially in CD (p = 0.02) (Figure 1). In dysbiosis situation, one luxR receptor gene from Bacteroides fragilis appeared to be over-expressed (p = 0.04) compared to non-dysbiotic patients (Figure 2). Conclusion Through this computational approach, AHL-synthesising bacteria have not been found. However, the expression of quorum sensing receptor genes appears to be modulated by IBD-associated gut dysbiosis. The role of LuxR receptors, especially in Bacteroides species, should be investigated to understand its impact on gut microbiota (Figure 3). Targeting LuxR receptors of bacterial quorum sensing might represent a new approach to modulate the gut microbiota in IBD.

Evidence challenging the causal role of gut microbiota in inflammatory bowel diseases.

Evidence challenging the causal role of gut microbiota in inflammatory bowel diseases.

Impact of IBD-Associated Dysbiosis on Bacterial Quorum Sensing Mediated by Acyl-Homoserine Lactone in Human Gut Microbiota

Intestinal dysbiosis is a key feature in the pathogenesis of inflammatory bowel disease (IBD). Acyl-homoserine lactones (AHL) are bacterial quorum-sensing metabolites that may play a role in the changes in host cells-gut microbiota interaction observed during IBD. The objective of our study was to investigate the presence and expression of AHL synthases and receptor genes in the human gut ecosystem during IBD. We used an in silico approach, applied to the Inflammatory Bowel Disease Multi'omics Database comprising bacterial metagenomic and metatranscriptomic data from stools of patients with Crohn's disease (CD) (n = 50), ulcerative colitis (UC) (n = 27) and non-IBD controls (n = 26). No known putative AHL synthase gene was identified; however, several putative luxR receptors were observed. Regarding the expression of these receptor genes, the luxR gene from Bacteroides dorei was under-expressed in IBD patients (p = 0.02) compared to non-IBD patients, especially in CD patients (p = 0.02). In the dysbiosis situation, one luxR receptor gene from Bacteroides fragilis appeared to be over-expressed (p = 0.04) compared to that of non-dysbiotic patients. Targeting LuxR receptors of bacterial quorum sensing might represent a new approach to modulate the gut microbiota in IBD.

Increased Primary Bile Acids with Ileocolonic Resection Impact Ileal Inflammation and Gut Microbiota in Inflammatory Bowel Disease.

Most Crohn's disease [CD] patients require surgery. Ileitis recurs after most ileocolectomies and is a critical determinant for outcomes. The impacts of ileocolectomy-induced bile acid [BA] perturbations on intestinal microbiota and inflammation are unknown. We characterized the relationships between ileocolectomy, stool BAs, microbiota and intestinal inflammation in inflammatory bowel disease [IBD]. Validated IBD clinical and endoscopic assessments were prospectively collected. Stool primary and secondary BA concentrations were compared based on ileocolectomy and ileitis status. Primary BA thresholds for ileitis were evaluated. Metagenomic sequencing was use to profile microbial composition and function. Relationships between ileocolectomy, BAs and microbiota were assessed. In 166 patients, elevated primary and secondary BAs existed with ileocolectomy. With ileitis, only primary BAs [795 vs 398 nmol/g, p = 0.009] were higher compared to without ileitis. The optimal primary BA threshold [≥228 nmol/g] identified ileitis on multivariable analysis [odds ratio = 2.3, p = 0.04]. Microbial diversity, Faecalibacterium prausnitzii and O-acetylhomoserine aminocarboxypropyltransferase [MetY] were decreased with elevated primary BAs. Amongst ileocolectomy patients, only those with elevated primary BAs had diversity, F. prausnitzii and MetY reductions. Those with both ileocolectomy and intermediate [p = 0.002] or high [≥228 nmol/g, p = 9.1e-11]] primary BA concentrations had reduced F. prausnitzii compared to without ileocolectomy. Those with ileocolectomy and low [<29.2 nmol/g] primary BA concentrations had similar F. prausnitzii to those without ileocolectomy [p = 0.13]. MetY was reduced with ileitis [p = 0.02]. Elevated primary BAs were associated with ileitis, and reduced microbial diversity, F. prausnitzii abundance and enzymatic abundance of MetY [acetate and l-methionine-producing enzyme expressed by F. prausnitzii], and were the only factors associated with these findings after ileocolectomy.

Quantitative Fecal Microbiota Profiles Relate to Therapy Response During Induction With Tumor Necrosis Factor α Antagonist Infliximab in Pediatric Inflammatory Bowel Disease.

The role of intestinal microbiota in inflammatory bowel diseases is intensively researched. Pediatric studies on the relation between microbiota and treatment response are sparse. We aimed to determine whether absolute abundances of gut microbes characterize the response to infliximab induction in pediatric inflammatory bowel disease. We recruited pediatric patients with inflammatory bowel disease introduced to infliximab at Children's Hospital, University of Helsinki. Stool samples were collected at 0, 2, and 6 weeks for microbiota and calprotectin analyses. We defined treatment response as fecal calprotectin value <100 µg/g at week 6. Intestinal microbiota were analyzed by 16S ribosomal RNA gene amplicon sequencing using the Illumina MiSeq platform. We analyzed total bacterial counts using quantitative polymerase chain reaction and transformed the relative abundances into absolute abundances based on the total counts. At baseline, the intestinal microbiota in the treatment responsive group (n = 10) showed a higher absolute abundance of Bifidobacteriales and a lower absolute abundance of Actinomycetales than nonresponders (n = 19). The level of inflammation according to fecal calprotectin showed no statistically significant association with the absolute abundances of fecal microbiota. The results on relative abundances differed from the absolute abundances. At the genus level, the responders had an increased relative abundance of Anaerosporobacter but a reduced relative abundance of Parasutterella at baseline. High absolute abundance of Bifidobacteriales in the gut microbiota of pediatric patients reflects anti-inflammatory characteristics associated with rapid response to therapy. This warrants further studies on whether modification of pretreatment microbiota might improve the outcomes.

Vitamin-Microbiota Crosstalk in Intestinal Inflammation and Carcinogenesis.

Inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC) are common diseases of the digestive system. Vitamin deficiencies and gut microbiota dysbiosis have a close relationship with the risk, development, and progression of IBD and CAC. There is a strong link between vitamins and the gut microbiome. Vitamins are extremely crucial for maintaining a healthy gut microbiota, promoting growth and development, metabolism, and innate immunity. Gut microbiota can not only influence the transport process of vitamins, but also produce vitamins to compensate for insufficient food intake. Emerging evidence suggests that oral vitamin supplementation can reduce inflammation levels and improve disease prognosis. In addition, improving the diet structure and consuming foods rich in vitamins not only help to improve the vitamin deficiency, but also help to reduce the risk of IBD. Fecal microbiota transplantation (FMT) and the application of vitamin-producing probiotics can better assist in the treatment of intestinal diseases. In this review, we discuss the interaction and therapeutic roles of vitamins and gut microbiota in IBD and CAC. We also summarize the methods of treating IBD and CAC by modulating vitamins. This may highlight strategies to target gut-microbiota-dependent alterations in vitamin metabolism in the context of IBD and CAC therapy.

Modulation of intestinal immune cell responses by eubiotic or dysbiotic microbiota in inflammatory bowel diseases

BackgroundAlterations of the gut microbiota have been linked to aberrant mucosal immune responses, leading to different intestinal and extraintestinal disorders, including inflammatory bowel diseases (IBD) in genetically susceptible hosts. Thus, restoration of immune homeostasis through the manipulation of the gut microbiota is now considered a possible therapeutic approach to treat IBD patients. Management of IBD patients is currently including the customization of microbe-targeted therapies, such as antibiotics, prebiotics, live biotherapeutics and faecal microbiota transplantation. In this narrative review, we will discuss recent advancements in the understanding of host-microbes interactions in IBD and the basis to promote homeostatic immune responses through microbe-targeted therapies. MethodsWe interrogated with no limit of publication time, the PubMed and Scopus databases using the following keywords: microbiota, inflammatory bowel diseases, IBD, immune system, microbe-targeted therapies. ResultsTherapeutic restoration of homeostatic immune function in IBD patients currently include the manipulation of the gut microbiota through antibiotics, prebiotics, probiotics, and faecal microbiota transplantation. Nonetheless, differences in efficacy has been reported according to existing microbe-targeted therapies, opening the venue for the search of novel approaches such as phage therapies and combinatorial therapies. ConclusionsAlterations in the composition of the gut microbiota have been implicated in a wide variety of pathologies, including IBD. Microbiome-modulating therapies have proven promising treatments targeting inflammation by modulating the microbiota to correct patients’ dysbiosis, normalize immune system responses and repair epithelial barrier deficiencies.