• Crohn’s disease
• Escherichia coli
• Mycobacterium avium paratuberculosis
• antibiotic therapy

• Escherichia coli
• Antibiotics
• Antimicrobial agents
• Antitubercular therapy
• Crohn’s disease
• Gastrointestinal tuberculosis
• Ulcerative colitis

• Child
• Humans
• Colitis, Ulcerative/diagnosis
• Crohn Disease/microbiology
• Anti-Bacterial Agents/therapeutic use
• Inflammatory Bowel Diseases/microbiology
• Rectal Fistula

• Humans
• Crohn Disease/epidemiology
• Crohn Disease/microbiology
• Crohn Disease/pathology
• Escherichia coli
• Escherichia coli Infections/epidemiology
• Escherichia coli Infections/microbiology
• Escherichia coli Infections/pathology
• Bacterial Adhesion
• Intestinal Mucosa/microbiology
• Intestinal Mucosa/pathology

• inflammatory bowel diseases
• prebiotics
• probiotics
• synbiotics
• therapeutic uses
• ulcerative colitis

• Humans
• Prebiotics
• Synbiotics
• Colitis, Ulcerative/therapy
• Probiotics/therapeutic use
• Inflammatory Bowel Diseases/microbiology

• Crohn's disease
• early biologics
• meta-analysis
• mucosal healing
• relapse
• remission

• Adolescent
• Child
• Humans
• Crohn Disease/drug therapy
• Immunosuppressive Agents/therapeutic use
• Remission Induction
• Biological Therapy
• Recurrence

• STAT3
• Ulcerative colitis
• ethanol
• immune cells
• inflammation
• probiotics

• Mice
• Animals
• Dextran Sulfate/toxicity
• Lactobacillus delbrueckii
• Colitis/pathology
• Colon/pathology
• Colitis, Ulcerative/chemically induced
• Colitis, Ulcerative/pathology
• Disease Models, Animal
• Ethanol/adverse effects
• Weight Loss
• Mice, Inbred C57BL
• Interleukin-22

• F30 AA027442 NIAAA NIH HHS
• F30 DK123929 NIDDK NIH HHS
• R21 AA025806 NIAAA NIH HHS
• T32 AA013527 NIAAA NIH HHS

• inflammatory bowel disease
• microbiome
• radiation
• radiotherapy

• bile acids and salts
• inflammatory bowel diseases
• microbiome-based therapy
• probiotics
• urolithin A

• Adult
• Child
• Humans
• Inflammatory Bowel Diseases/pathology
• Gastrointestinal Microbiome
• Fecal Microbiota Transplantation/methods
• Colitis, Ulcerative/therapy
• Colitis, Ulcerative/complications

Previous studies have shown that antibiotic use and enterocolitis increase the risk of developing inflammatory bowel disease (IBD) in western countries. However, these risk factors have not yet been identified in Asian populations. This study aimed to investigate the risk of IBD development associated with antibiotic use and enterocolitis in Japan. A Japanese health insurance claims database was used to identify patients recently diagnosed with Crohn’s disease (CD) and ulcerative colitis (UC) along with five matched participants without IBD. Episodes of antibiotic use and enterocolitis for 1 and 2 years before the date of diagnosis were analyzed using a conditional regression test. A total of 371 patients with CD and 2420 with UC were included. The adjusted odds ratio (AOR) increased in association with antibiotic use to 1.61 (95% confidence interval [CI] 1.26–2.05) and 1.20 (95% CI 1.09–1.31) and enterocolitis to 3.40 (95% CI 2.60–4.44) and 2.14 (95% CI 1.88–2.43) in 1 year in CD and UC, respectively. The risk associated with antibiotics was independent of the number or type of antibiotics, and the risk associated with enterocolitis did not differ with the pathogen that caused the disease. However, prior exposure to antibiotic use and enterocolitis was associated with an increased risk of developing IBD.

Within the IBD entity of Crohn's disease, there is currently no differentiation between ileal and colonic manifestation for recruitment of patients in clinical trials, well-powered analysis of study results or therapeutic decisions in daily clinical practice. However, there is accumulating evidence from epidemiological, genetic, microbial, immunological, and clinical characteristics that clearly indicate that ileal Crohn's disease represents a distinct disease entity, which differentiates itself from colonic Crohn's disease. This is also reflected by lower efficacy of targeted therapies in isolated ileal compared to colonic Crohn's disease. The distinct site-specific mechanisms that drive heightened non-response in ileal disease need to be analysed in-depth in the future, to enable optimized therapy in the individual Crohn's disease patient.

• Adalimumab
• Crohn’s disease
• Infliximab
• Tofacitinib
• Ulcerative colitis
• Ustekinumab
• Vedolizumab

• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/epidemiology
• Colitis, Ulcerative/therapy
• Consensus
• Crohn Disease
• Humans
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/epidemiology
• Inflammatory Bowel Diseases/therapy
• United Arab Emirates/epidemiology

Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases of the gastrointestinal and respiratory tracts, respectively. These mucosal tissues bear commonalities in embryology, structure and physiology. Inherent similarities in immune responses at the two sites, as well as overlapping environmental risk factors, help to explain the increase in prevalence of IBD amongst COPD patients. Over the past decade, a tremendous amount of research has been conducted to define the microbiological makeup of the intestine, known as the intestinal microbiota, and determine its contribution to health and disease. Intestinal microbial dysbiosis is now known to be associated with IBD where it impacts upon intestinal epithelial barrier integrity and leads to augmented immune responses and the perpetuation of chronic inflammation. While much less is known about the lung microbiota, like the intestine, it has its own distinct, diverse microflora, with dysbiosis being reported in respiratory disease settings such as COPD. Recent research has begun to delineate the interaction or crosstalk between the lung and the intestine and how this may influence, or be influenced by, the microbiota. It is now known that microbial products and metabolites can be transferred from the intestine to the lung via the bloodstream, providing a mechanism for communication. While recent studies indicate that intestinal microbiota can influence respiratory health, intestinal dysbiosis in COPD has not yet been described although it is anticipated since factors that lead to dysbiosis are similarly associated with COPD. This review will focus on the gut-lung axis in the context of IBD and COPD, highlighting the role of environmental and genetic factors and the impact of microbial dysbiosis on chronic inflammation in the intestinal tract and lung.

• Crohn's disease metabolites
• chronic obstructive pulmonary disease
• gut-lung axis
• inflammatory bowel disease
• microbial dysbiosis

• Adalimumab/administration & dosage
• Adalimumab/adverse effects
• Anti-Inflammatory Agents/administration & dosage
• Anti-Inflammatory Agents/adverse effects
• Cognitive Behavioral Therapy
• Electroacupuncture
• Exercise
• Fatigue/etiology
• Fatigue/therapy
• Fatty Acids, Omega-3/administration & dosage
• Fatty Acids, Omega-3/adverse effects
• Ferric Compounds/adverse effects
• Hematinics/adverse effects
• Humans
• Inflammatory Bowel Diseases/complications
• Psychotherapy, Brief
• Pyrones/adverse effects
• Quality of Life
• Randomized Controlled Trials as Topic

• antibiotics
• crohn’s disease
• inflammatory bowel disease
• key points
• probiotics
• ulcerative colitis

Psoriatic patients have altered microbiota, both in the intestine and on the skin. It is not clear, however, whether this is a cause or consequence of the disease. In this study, using an experimental mouse model of psoriasis induced by imiquimod (IMQ), we show that oral treatment with a broad spectrum of antibiotics (MIX) or metronidazole (MET) alone mitigates the severity of skin inflammation through downregulation of Th17 immune response in conventional mice. Since some antibiotics, including MET, can influence immune system reactivity, we also evaluated the effect of MIX in the same model under germ-free (GF) conditions. GF mice treated with MET did not show milder signs of imiquimod-induced skin inflammation (IISI) which supports the conclusion that the therapeutic effect is mediated by changes in microbiota composition. Moreover, compared to controls, mice treated with MIX had a significantly higher abundance of the genus Lactobacillus in the intestine and on the skin. Mice treated with MET had a significantly higher abundance of the genera Bifidobacterium and Enterococcus both on the skin and in the intestine and of Parabacteroides distasonis in the intestine. Additionally, GF mice and mice monocolonized with either Lactobacillus plantarum or segmented filamentous bacteria (SFB) were more resistant to IISI than conventional mice. Interestingly, compared to GF mice, IMQ induced a higher degree of systemic Th17 activation in mice monocolonized with SFB but not with L. plantarum. The present findings provide evidence that intestinal and skin microbiota directly regulates IISI and emphasizes the importance of microbiota in the pathogenesis of psoriasis.

• animal model
• antibiotics
• germ-free
• imiquimod
• intestine
• microbiota
• psoriasis
• skin

• Anti-Bacterial Agents/adverse effects
• Anti-Bacterial Agents/therapeutic use
• Crohn Disease/drug therapy
• Humans
• Induction Chemotherapy/methods
• Maintenance Chemotherapy/methods
• Randomized Controlled Trials as Topic

• antibiotics
• azithromycin
• crohn’s disease
• inflammatory bowel disease
• paediatric
• therapy

• Inflammatory bowel disease (IBD)
• antibiotics

• Gut microbiome
• arterial hypertension
• gut flora
• microorganisms
• prebiotics
• probiotics
• short chain fatty acids.

• Animals
• Antihypertensive Agents/therapeutic use
• Arterial Pressure/drug effects
• Bacteria/drug effects
• Bacteria/growth & development
• Disease Models, Animal
• Dysbiosis
• Gastrointestinal Microbiome/drug effects
• Host-Pathogen Interactions
• Humans
• Hypertension/drug therapy
• Hypertension/epidemiology
• Hypertension/microbiology
• Hypertension/physiopathology
• Intestines/microbiology
• Probiotics/therapeutic use
• Risk Factors

• CROHN'S COLITIS

Inflammatory bowel disease is thought to be caused by an aberrant immune response to gut bacteria in a genetically susceptible host. The gut microbiota plays an important role in the pathogenesis and complications of the two main inflammatory bowel diseases: Crohn’s disease (CD) and ulcerative colitis. Alterations in gut microbiota, and specifically reduced intestinal microbial diversity, have been found to be associated with chronic gut inflammation in these disorders. Specific bacterial pathogens, such as virulent Escherichia coli strains, Bacteroides spp, and Mycobacterium avium subspecies paratuberculosis, have been linked to the pathogenesis of inflammatory bowel disease. Antibiotics may influence the course of these diseases by decreasing concentrations of bacteria in the gut lumen and altering the composition of intestinal microbiota. Different antibiotics, including ciprofloxacin, metronidazole, the combination of both, rifaximin, and anti-tuberculous regimens have been evaluated in clinical trials for the treatment of inflammatory bowel disease. For the treatment of active luminal CD, antibiotics may have a modest effect in decreasing disease activity and achieving remission, and are more effective in patients with disease involving the colon. Rifamixin, a non absorbable rifamycin has shown promising results. Treatment of suppurative complications of CD such as abscesses and fistulas, includes drainage and antibiotic therapy, most often ciprofloxacin, metronidazole, or a combination of both. Antibiotics might also play a role in maintenance of remission and prevention of post operative recurrence of CD. Data is more sparse for ulcerative colitis, and mostly consists of small trials evaluating ciprofloxacin, metronidazole and rifaximin. Most trials did not show a benefit for the treatment of active ulcerative colitis with antibiotics, though 2 meta-analyses concluded that antibiotic therapy is associated with a modest improvement in clinical symptoms. Antibiotics show a clinical benefit when used for the treatment of pouchitis. The downsides of antibiotic treatment, especially with recurrent or prolonged courses such as used in inflammatory bowel disease, are significant side effects that often cause intolerance to treatment, Clostridium dificile infection, and increasing antibiotic resistance. More studies are needed to define the exact role of antibiotics in inflammatory bowel diseases.

• Antibiotic treatment
• Inflammatory bowel disease
• Ulcerative colitis
• Crohn’s disease

• Animals
• Anti-Bacterial Agents/adverse effects
• Anti-Bacterial Agents/therapeutic use
• Bacteria/drug effects
• Bacteria/immunology
• Bacteria/pathogenicity
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/immunology
• Colitis, Ulcerative/microbiology
• Crohn Disease/drug therapy
• Crohn Disease/immunology
• Crohn Disease/microbiology
• Gastrointestinal Microbiome/drug effects
• Host-Pathogen Interactions
• Humans
• Intestines/drug effects
• Intestines/immunology
• Intestines/microbiology
• Practice Guidelines as Topic
• Treatment Outcome

• Administration, Oral
• Adrenal Cortex Hormones/therapeutic use
• Anti-Inflammatory Agents/administration & dosage
• Anti-Inflammatory Agents/adverse effects
• Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
• Budesonide/administration & dosage
• Budesonide/adverse effects
• Crohn Disease/drug therapy
• Humans
• Induction Chemotherapy/methods
• Mesalamine/therapeutic use
• Randomized Controlled Trials as Topic

• Crohn disease
• anti-bacterial agents
• ciprofloxacin
• inflammatory bowel diseases
• meta-analysis

• Crohn's disease
• ciprofloxacin
• meta-analysis

The development of culture-independent techniques and next-generation sequencing has led to a staggering rise in the number of microbiome studies over the last decade. Although it remains important to identify the taxa of microbes present in a variety of environmental samples, including the gut microbiomes of healthy and diseased individuals, the next stage of microbiome research will need to focus on uncovering the role of the microbiome rather than its mere composition. Here, we introduce techniques that go beyond identifying the taxa present within a sample and examine the biological function of the microbiome or the host-microbiome interaction.

Ulcerative colitis and Crohn’s disease, commonly known as inflammatory bowel disease (IBD), draw attention from specialists of various disorders, including gastroenterology, psychiatry, and radiology. The involvement of a cortical influence in the brain-gut axis as well as the interaction of the hypothalamic-pituitary-adrenal axis and the peripheral nervous system provide an initial explanation of the psychological symptoms associated with IBD. The involvement of structures the limbic system, such as the anterior cingulate cortex, the prefrontal cortex, and the amygdala, paves the way for the discovery of the mechanisms underlying depression depression, anxiety, alexithymia, personality traits, and other psychological impairments following the onset of IBD. Psychiatric therapy in IBD patients is almost as important as the gastroenterological approach and consists of pharmacological treatment and psychotherapy. Neither of the available psychiatric treatment methods is considered the golden standard because both methods have side effects, and psychotropic medication can provoke the worsening of IBD symptoms. Thus, both approaches must be applied with awareness of the possibility of side effects. We suggest that psychiatrists and gastroenterologists work together to reach a consensus on IBD therapy to ensure success and to reduce side effects and relapse to the lowest possible rates.

• Inflammatory bowel disease
• Psychiatry
• Treatment
• Personality traits
• Depression
• Anxiety

• Adolescent
• Adult
• Anxiety/complications
• Cognition Disorders/complications
• Comorbidity
• Depression/complications
• Humans
• Inflammatory Bowel Diseases/complications
• Inflammatory Bowel Diseases/psychology
• Inflammatory Bowel Diseases/therapy
• Mental Disorders/complications
• Mental Disorders/therapy
• Personality
• Psychotherapy/methods
• Quality of Life
• Recurrence
• Severity of Illness Index
• Sleep Deprivation

Crohn's disease (CD) is one of the two major forms of inflammatory bowel disease (IBD). Although the etiology of CD is unclear, many experimental and clinical observations support the potential role for intestinal microflora in the pathogenesis of CD. Manipulation of the luminal content using antibiotics may therefore represent a potentially effective therapeutic option. Some randomized controlled trials have demonstrated the efficacy of these drugs in treating the perianal disease, inducing and maintaining of CD remission and decreasing CD recurrence rates in operated patients. But, the use of antibacterial therapy for CD is also controversial, even this approach is frequently and successfully adopted in clinical practice. Fairly narrow indications for antibiotics are suggested by current management guidelines. Large studies are required to better define the role of antibacterial agents and combination regimens in CD. Broad-spectrum antibiotics, such as metronidazole, fluoroquinolones and rifaximin, are widely used to treat CD, and their effects have been recognized. Because of the lack of adequate theoretical support and adverse drug reactions, the reasonable application of antibiotics to treat CD is still a clinical problem.

• Antibiotics
• Crohn's disease
• Gut microbiota
• Metronidazole
• Ciprofloxacin
• Rifaximin

While antimicrobials are clinically effective in preventing post-operative recurrence, the role for antibiotics in primary therapy for Crohn’s disease (CD) remains unclear. The recent multicenter phase 2 trial by Prantera et al received wide attention because it demonstrated an increase in the week 12 remission rate in patients with moderately active CD treated with rifaximin and renewed interest in microbial manipulation as primary therapy for CD. In this commentary, we discuss aspects of durability, immune cell polarization, and safety of microbial manipulation as primary therapy for CD.

• Inflammatory bowel disease
• Rifaximin
• Microbiome

Many data coming from animal models and clinical observations support an involvement of intestinal microbiota in the pathogenesis of Crohn’s disease (CD). It is hypothesized in fact, that the development of chronic intestinal inflammation is caused by an abnormal immune response to normal flora in genetically susceptible hosts. The involvement of bacteria in CD inflammation has provided the rationale for including antibiotics in the therapeutic armamentarium. However, randomized controlled trials have failed to demonstrate an efficacy of these drugs in patients with active uncomplicated CD, even if a subgroup of patients with colonic location seems to get benefit from antibiotics. Nitroimidazole compounds have been shown to be efficacious in decreasing CD recurrence rates in operated patients, and the use of metronidazole and ciprofloxacin is recommended in perianal disease. However, the appearance of systemic side effects limits antibiotic long-term employment necessary for treating a chronic relapsing disease. Rifaximin, characterized by an excellent safety profile, has provided promising results in inducing remission of CD.

• Antibiotics
• Crohn’s disease
• Gut microbiota
• Mycobacteria

• crohn’s disease
• guidelines
• practice guidelines
• evidence
• consensus

• Crohn Disease/complications
• Crohn Disease/diagnosis
• Crohn Disease/therapy
• Evidence-Based Practice
• Humans
• Japan