• AAD, Antibiotic-Associated Diarrhea
• AIDS, Acquired Immunodeficiency Syndrome
• AIEC, Adherent-Invasive Escherichia Coli
• APC, Antigen-Presenting Cells
• ART, Antiretroviral Therapy
• CARD15, Caspase Recruitment Domain–Containing Protein 15
• CARD9, Caspase Recruitment Domain–Containing Protein 9
• CAZymes, Carbohydrate-Active Enzymes
• CCL4, C-C Motif Chemokine Ligand 4
• CCR5, C-C Chemokine Receptor Type 5
• CD, Cluster Of Differentiation
• CD, Crohn’s Disease
• CRC, Colorectal Cancer
• CXCR4, C-X-C Chemokine Receptor Type 4
• Crohn’s disease
• DC, Dendritic Cells
• DC-SIGN, Dendritic Cell–Specific Intercellular Adhesion Molecule-3–Grabbing Non-Integrin
• ERS, Endoplasmic Reticulum Stress
• FMT, Fecal Microbiota Transplantation
• FVT, Fecal Virome Transplantation
• GIT, Gastrointestinal Tract
• HIV
• HIV, Human Immunodeficiency Virus
• IBD, Inflammatory Bowel Disease
• IFABP, Intestinal Fatty Acid–Binding Protein
• IL, Interleukin
• ILCs, Innate Lymphoid Cells
• MALT, Mucosa-Associated Lymphoid Tissue
• MAMP, Microbe-Associated Molecular Pattern
• NF-κB, Nuclear Factor Kappa B
• NK, Natural Killer Cells
• NOD2, Nucleotide-Binding Oligomerization Domain–Containing Protein 2
• NOS, Nitric Oxide Synthase
• PPAR-γ, Peroxisome Proliferator-Activated Receptor Gamma
• PRR, Pattern Recognition Receptor
• SCFA, Short-Chain Fatty Acids
• SLE, Systemic Lupus Erythematosus
• TGF-β, Transforming Growth Factor–β
• TLR, Toll-Like Receptor
• TNF-α, Tumor Necrosis Factor–α
• Th17, T Helper 17 Cells
• UC, Ulcerative Colitis
• gut microbiota
• pDC, Plasmacytoid Dendritic Cells
• probiotics
• sCD14, Soluble CD14

• Humans
• Crohn Disease/therapy
• Crohn Disease/complications
• Crohn Disease/immunology
• HIV Infections/complications
• HIV Infections/immunology
• Disease Progression
• Probiotics/therapeutic use
• Gastrointestinal Microbiome

• Crohn's disease
• fecal microbiota transplantation
• network meta‐analysis
• prebiotics
• probiotics
• synbiotics
• ulcerative colitis

• Humans
• Gastrointestinal Microbiome
• Probiotics/therapeutic use
• Probiotics/administration & dosage
• Fecal Microbiota Transplantation/methods
• Prebiotics/administration & dosage
• Synbiotics/administration & dosage
• Treatment Outcome
• Colitis, Ulcerative/therapy
• Colitis, Ulcerative/microbiology
• Inflammatory Bowel Diseases/therapy
• Inflammatory Bowel Diseases/microbiology
• Crohn Disease/therapy
• Crohn Disease/microbiology
• Randomized Controlled Trials as Topic
• Combined Modality Therapy
• Remission Induction

• 2021YFA1301300 National Key Research and Development Program of China
• 82170557 National Natural Science Foundation of China

• Green approach
• Microbeads
• Probiotics
• Simulated gastrointestinal conditions
• Starch nanoparticles
• Viability

• Probiotics/chemistry
• Starch/chemistry
• Lacticaseibacillus rhamnosus/chemistry
• Nanoparticles/chemistry
• Digestion
• Microbial Viability
• Microspheres
• Capsules
• X-Ray Diffraction
• Particle Size
• Spectroscopy, Fourier Transform Infrared

• Alteration of intestinal flora
• Biologic therapy
• Genetic predisposition
• Herbal treatment
• Immune dysregulation
• Ulcerative colitis (UC)

• Humans
• Colitis, Ulcerative/therapy
• Colitis, Ulcerative/immunology
• Gastrointestinal Microbiome
• Fecal Microbiota Transplantation
• Probiotics/therapeutic use
• Animals

• Crohn's disease
• RCT
• clinical outcomes
• clinical remission
• endoscopic response
• inflammatory bowel disease
• microbiome modulation
• probiotic
• recurrence
• ulcerative colitis

• Humans
• Colitis, Ulcerative/therapy
• Colitis, Ulcerative/immunology
• Crohn Disease/immunology
• Crohn Disease/therapy
• Pouchitis/immunology
• Pouchitis/therapy
• Probiotics/administration & dosage
• Probiotics/adverse effects
• Randomized Controlled Trials as Topic
• Recurrence
• Remission Induction
• Systematic Reviews as Topic
• Treatment Outcome

• gut microbiome
• ibd
• immune dysregulation
• inflammatory bowel disease
• treatment strategies

• Immunological response
• Microorganisms
• Regeneration
• Tissue repair

• Humans
• Immunity
• Wound Healing
• Regenerative Medicine
• Immune System
• Skin

• Humans
• Cholangitis, Sclerosing/therapy

• Crohn’s disease
• Diet
• Inflammatory bowel disease
• Nutrition
• Treatment
• Ulcerative colitis

Ulcerative colitis (UC) belongs to the group of inflammatory bowel diseases (IBD). UC is an incurable, diffuse, and chronic inflammatory process of the colonic mucosa with alternating periods of exacerbation and remission. This review aimed to analyze the scientific research conducted to date to determine what impact different nutritional plans and dietary supplements may have on the course of UC. The latest 98 articles about nutrition and supplementation in ulcerative colitis were used to prepare the work. Certain components in food can greatly influence the course of UC, inducing changes in the composition and function of the gut microbiome. This activity may be an important part of therapy for people with IBD. The Mediterranean diet has shown the most promising results in the treatment of patients with UC due to its high content of biologically active foods. Patients with UC may benefit from the UC Exclusion Diet (UCED); however, it is a new nutritional plan that requires further research. Patents frequently resort to unconventional diets, which, because of their frequent elimination of nutrient-rich foods, can worsen the health and nutritional status of those who follow them. The benefits of omega-3 fatty acids and probiotics supplementation may have additional therapeutic effects; however, the evidence is not unequivocal.

• FODMAP
• Mediterranean diet
• SCD
• UCED
• colitis ulcerosa
• diet
• supplements
• ulcerative colitis

• FODMAP diet
• IBD
• Mediterranean diet
• gluten
• lactose
• nutrition
• pediatric patient

• Adult
• Child
• Colitis, Ulcerative
• Crohn Disease
• Diet
• Diet, Mediterranean
• Humans
• Inflammatory Bowel Diseases/complications
• Nutritional Status

• engineered microbiome
• fecal microbiome transplantation
• human microbiome
• microbiome therapeutics
• prebiotics
• probiotics

• Gut microbiota
• Inflammatory bowel disease
• Prebiotics
• Probiotics
• Remission
• Synbiotics

• Gastrointestinal Microbiome
• Humans
• Inflammatory Bowel Diseases/therapy
• Prebiotics
• Probiotics
• Synbiotics

• 31372453 National Natural Science Foundation of China
• 152102310260 Science and Technology Department of Henan Province

• Anti-inflammatory diet
• Inflammatory bowel disease
• Nutritional intake
• Relapse
• Remission

(1) Background: Inflammatory bowel diseases are pathologies of unknown etiology and auto-immune pathogenia. The use of probiotics is studied in order to increase the arsenal of treatments. The aim was to assess the efficacy of the probiotics in these diseases in the active or quiescent phases; (2) Methods: A systematic review with meta-analysis was performed by an exhaustive bibliographic search in Medline, Cinahl, Embase, Scopus, Web of Science, and Cochrane Library. The inclusion criteria were studies of more than 10 years, English/Spanish, clinical trials, and involving human beings. Relative risk was used to compare efficacy, which was meta-analyzed using a fixed effects model. Heterogeneity was evaluated with the Higgins I² test; (3) Results: Nineteen studies were included in the systematic review and 17 in the meta-analysis, with a total of 1537 patients (n_{experimental group} = 762; n_{placebo group} = 775). There are significant remission differences in ulcerative colitis (relative risk (RR) = 0.81; 95% CI = 0.72–0.91; I² = 32%; p = 0.16). However, no significant differences were found in the use of probiotics for the prevention of ulcerative colitis, and for the remission of Crohn’s disease; (4) Conclusions: There are data showing an additional beneficial effect of probiotics on active ulcerative colitis. More and better studies are needed which assess its possible therapeutic efficacy for quiescent ulcerative colitis and for Crohn’s disease.

• Crohn’s disease
• efficacy
• inflammatory bowel disease
• probiotics
• ulcerative colitis

• Adult
• Combined Modality Therapy/methods
• Humans
• Inflammatory Bowel Diseases/drug therapy
• Probiotics/pharmacology
• Treatment Outcome

• Alginate
• In vitro/in situviability
• Lactobacillus
• Nanoencapsulation by electrospinning
• simulated gastrointestinal conditions

• Crohn's disease
• Enteral nutrition
• Inflammatory bowel disease
• Nutritional therapy
• Parenteral nutrition
• Ulcerative colitis

• 5-ASA
• Guidance
• Mucosal Healing
• TNF

Liver, pancreatic, and inflammatory bowel diseases are often associated with nutritional difficulties and necessitate an adequate nutritional therapy in order to support the medical treatment. As most patients with non-alcoholic fatty liver disease are overweight or obese, guidelines recommend weight loss and physical activity to improve liver enzymes and avoid liver cirrhosis. In contrast, patients with alcoholic steatohepatitis or liver cirrhosis have a substantial risk for protein depletion, trace elements deficiency, and thus malnutrition. Patients with chronic pancreatitis and patients with inflammatory bowel disease have a similar risk for malnutrition. Therefore, it clearly is important to screen these patients for malnutrition with established tools and initiate adequate nutritional therapy. If energy and protein intake are insufficient with regular meals, oral nutritional supplements or artificial nutrition, i.e., tube feeding or parenteral nutrition, should be used to avoid or treat malnutrition. However, the oral route should be preferred over enteral or parenteral nutrition. Acute liver failure and acute pancreatitis are emergencies, which require close monitoring for the treatment of metabolic disturbances. In most patients, energy and protein requirements are increased. In acute pancreatitis, the former recommendation of fasting is obsolete. Each disease is discussed in this manuscript and special recommendations are given according to the pathophysiology and clinical routine.

• artificial nutrition
• inflammation
• malnutrition
• micronutrient deficiency
• monitoring
• oral nutritional supplements

The role of the microbiome in health and human disease has emerged at the forefront of medicine in the 21st century. Over the last 2 decades evidence has emerged to suggest that inflammation-derived oxidative damage and cytokine induced toxicity may play a significant role in the neuronal damage associated with Parkinson’s disease (PD). Presence of pro-inflammatory cytokines and T cell infiltration has been observed in the brain parenchyma of patients with PD. Furthermore, evidence for inflammatory changes has been reported in the enteric nervous system, the vagus nerve branches and glial cells. The presence of α-synuclein deposits in the post-mortem brain biopsy in patients with PD has further substantiated the role of inflammation in PD. It has been suggested that the α-synuclein misfolding might begin in the gut and spread “prion like” via the vagus nerve into lower brainstem and ultimately to the midbrain; this is known as the Braak hypothesis. It is noteworthy that the presence of gastrointestinal symptoms (constipation, dysphagia, and hypersalivation), altered gut microbiota and leaky gut have been observed in PD patients several years prior to the clinical onset of the disease. These clinical observations have been supported by in vitro studies in mice as well, demonstrating the role of genetic (α-synuclein overexpression) and environmental (gut dysbiosis) factors in the pathogenesis of PD. The restoration of the gut microbiome in patients with PD may alter the clinical progression of PD and this alteration can be accomplished by carefully designed studies using customized probiotics and fecal microbiota transplantation.

• Dysbiosis
• Fecal microbiota transplantation
• Microbiota
• Parkinson disease
• Probiotics

Within the last century, human lifestyle and dietary behaviors have changed dramatically. These changes, especially concerning hygiene, have led to a marked decrease in some diseases, i.e., infectious diseases. However, other diseases that can be attributed to the so-called ‘Western’ lifestyle have increased, i.e., metabolic and cardiovascular disorders. More recently, multifactorial disorders, such as autoimmune and neurodegenerative diseases, have been associated with changes in diet and the gut microbiome. In particular, short chain fatty acid (SCFA)-producing bacteria are of high interest. SCFAs are the main metabolites produced by bacteria and are often reduced in a dysbiotic state, causing an inflammatory environment. Based on advanced technologies, high-resolution investigations of the abundance and composition of the commensal microbiome are now possible. These techniques enable the assessment of the relationship between the gut microbiome, its metabolome and gut-associated immune and neuronal cells. While a growing number of studies have shown the indirect impact of gut metabolites, mediated by alterations of immune-mediated mechanisms, the direct influence of these compounds on cells of the central nervous system needs to be further elucidated. For instance, the SCFA propionic acid (PA) increases the amount of intestine-derived regulatory T cells, which furthermore can positively affect the central nervous system (CNS), e.g., by increasing remyelination. However, the question of if and how PA can directly interact with CNS-resident cells is a matter of debate. In this review, we discuss the impact of an altered microbiome composition in relation to various diseases and discuss how the commensal microbiome is shaped, starting from the beginning of human life.

• dysbiosis
• gut–brain-axis
• microbiome
• multiple sclerosis
• neurodegeneration
• neuroinflammation
• short chain fatty acids

• Brain/metabolism
• Diet
• Dysbiosis
• Gastrointestinal Microbiome
• Humans
• Intestines/innervation
• Intestines/microbiology
• Neurodegenerative Diseases/etiology
• Neurodegenerative Diseases/metabolism
• Neurodegenerative Diseases/pathology
• Neuroimmunomodulation

• Anti-tumor necrosis factor-α
• Crohn's disease
• Inflammatory bowel disease
• Ulcerative colitis

• dysbiosis
• inflammatory mediators
• liver cirrhosis
• oral microbiota
• pancreatic cancer
• probiotics
• risk

• Clinical remission
• Medilac-S®
• Mesalazine
• Meta-analysis
• Sulfasalazine
• Systematic review
• Ulcerative colitis

• Crohn's disease
• Fecal microbiota transplantation
• Fecal transplant
• Inflammatory bowel disease
• Stool transplant
• Ulcerative colitis

Crohn’s disease (CD) is a lifelong illness with substantial morbidity, although new therapies and treatment paradigms have been developed. We provide guidance for treatment of ambulatory patients with mild to severe active luminal CD.

We performed a systematic review to identify published studies of the management of CD. The quality of evidence and strength of recommendations were rated according to the Grading of Recommendation Assessment, Development and Evaluation (GRADE) approach. Statements were developed through an iterative online platform and then finalized and voted on by a group of specialists.

The consensus includes 41 statements focused on 6 main drug classes: antibiotics, 5-aminosalicylate, corticosteroids, immunosuppressants, biologic therapies, and other therapies. The group suggested against the use of antibiotics or 5-aminosalicylate as induction or maintenance therapies. Corticosteroid therapies (including budesonide) can be used as induction, but not maintenance therapies. Among immunosuppressants, thiopurines should not be used for induction, but can be used for maintenance therapy for selected low-risk patients. Parenteral methotrexate was proposed for induction and maintenance therapy in patients with corticosteroid-dependent CD. Biologic agents, including tumor necrosis factor antagonists, vedolizumab, and ustekinumab, were recommended for patients failed by conventional induction therapies and as maintenance therapy. The consensus group was unable to clearly define the role of concomitant immunosuppressant therapies in initiation of treatment with a biologic agent.

Optimal management of CD requires careful patient assessment, acknowledgement of patient preferences, evidence-based use of existing therapies, and thorough assessment to define treatment success.

• 5-ASA
• Guidance
• Mucosal Healing
• TNF

• Encuesta
• Probiotics
• Probióticos
• Recomendaciones de probióticos
• Recommendations for probiotics
• Survey

Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. However, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation (FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in the pathogenesis and treatment of UC.

• Fecal microbiota transplantation
• Intestinal microbiota
• Ulcerative colitis
• Probiotics
• Mechanism
• Clinical application

• Animals
• Bacteria/growth & development
• Bacteria/immunology
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/immunology
• Colitis, Ulcerative/microbiology
• Colitis, Ulcerative/therapy
• Colon/immunology
• Colon/microbiology
• Fecal Microbiota Transplantation/adverse effects
• Gastrointestinal Microbiome
• Host-Pathogen Interactions
• Humans
• Probiotics/adverse effects
• Probiotics/therapeutic use
• Treatment Outcome

• Crohn disease
• Inflammation
• Inflammatory bowel disease
• Microbiome
• Microbiota
• Pouchitis
• Probiotic
• Ulcerative colitis

• cardiovascular disease
• diabetes
• gastrointestinal disease
• infections
• obesity
• probiotics

• Adultos
• Adults
• Children
• Consenso
• Consensus
• Enfermedades gastrointestinales
• Gastrointestinal diseases
• Mexico
• México
• Niños
• Probiotics
• Probióticos

• Adult
• Child
• Consensus
• Delphi Technique
• Gastroenterology
• Guidelines as Topic
• Humans
• Mexico
• Probiotics/therapeutic use

Diet has been speculated to be a factor in the pathogenesis of inflammatory bowel disease and may be an important factor in managing disease symptoms. Patients manipulate their diet in attempt to control symptoms, often leading to the adoption of inappropriately restrictive diets, which places them at risk for nutritional complications. Health professionals struggle to provide evidence-based nutrition guidance to patients due to an overall lack of uniformity or clarity amongst research studies. Well-designed diet studies are urgently needed to create an enhanced understanding of the role diet plays in the management of inflammatory bowel disease. The aim of this review is to summarize the current data available on dietary management of inflammatory bowel disease and to demonstrate that dietary modulation may be an important consideration in managing disease. By addressing the relevance of diet in inflammatory bowel disease, health professionals are able to better support patients and collaborate with dietitians to improve nutrition therapy.

• Crohn’s disease
• diet
• diet therapy
• inflammatory bowel disease
• nutrition
• nutrition therapy
• ulcerative colitis

• Databases, Factual
• Diet
• Evidence-Based Medicine
• Humans
• Inflammatory Bowel Diseases/diet therapy
• Meta-Analysis as Topic
• Nutritional Support
• Observational Studies as Topic
• Randomized Controlled Trials as Topic
• Recommended Dietary Allowances

• Crohn's disease
• Enteral nutrition
• Inflammatory bowel disease
• Nutritional therapy
• Parenteral nutrition
• Ulcerative colitis

• Humans
• Inflammatory Bowel Diseases/drug therapy
• Pouchitis/drug therapy
• Probiotics/therapeutic use
• Publications/standards
• Remission Induction

The cause of Crohn’s disease (CD) has posed a conundrum for at least a century. A large body of work coupled with recent technological advances in genome research have at last started to provide some of the answers. Initially this review seeks to explain and to differentiate between bowel inflammation in the primary immunodeficiencies that generally lead to very early onset diffuse bowel inflammation in humans and in animal models, and the real syndrome of CD. In the latter, a trigger, almost certainly enteric infection by one of a multitude of organisms, allows the faeces access to the tissues, at which stage the response of individuals predisposed to CD is abnormal. Direct investigation of patients’ inflammatory response together with genome-wide association studies (GWAS) and DNA sequencing indicate that in CD the failure of acute inflammation and the clearance of bacteria from the tissues, and from within cells, is defective. The retained faecal products result in the characteristic chronic granulomatous inflammation and adaptive immune response. In this review I will examine the contemporary evidence that has led to this understanding, and look for explanations for the recent dramatic increase in the incidence of this disease.

• Bacteria
• Crohn’s
• GWAS
• Gastroenteritis
• Gene
• Immunology
• Infection
• Inflammatory Bowel Disease

• Bacteria
• Crohn’s
• GWAS
• Gastroenteritis
• Gene
• Immunology
• Infection
• Inflammatory Bowel Disease

• Bacteriophage
• Host-bacteria interactions
• Microbial ecology
• Microbiome
• Synthetic biology

• Animals
• Anti-Infective Agents/therapeutic use
• Bioengineering
• Humans
• Microbiota
• Probiotics/therapeutic use

• P30 DK043351 NIDDK NIH HHS
• Howard Hughes Medical Institute
• R01 EB017755 NIBIB NIH HHS
• P50 GM098792 NIGMS NIH HHS
• DP2 OD008435 NIH HHS