• Inflammatory bowel disease
• epidemiology
• fatigue

• Humans
• Male
• Female
• Fatigue/etiology
• Fatigue/epidemiology
• Fatigue/diagnosis
• Remission Induction
• Adult
• Crohn Disease/complications
• Crohn Disease/drug therapy
• Crohn Disease/diagnosis
• Middle Aged
• Colitis, Ulcerative/complications
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/drug therapy
• Leukocyte L1 Antigen Complex/analysis
• Surveys and Questionnaires
• Severity of Illness Index
• Magnetic Resonance Imaging

• AB3526 Østfold Hospital Trust
• Takeda Pharmaceuticals
• Pfizer
• Tillotts Pharma
• the Dam Foundation
• the Southeastern Health Authorities

• CD
• Crohn's disease
• ERCP
• IBD
• UC
• Ulcerative colitis

• Humans
• Cholangiopancreatography, Endoscopic Retrograde/adverse effects
• Cholangiopancreatography, Endoscopic Retrograde/methods
• Retrospective Studies
• Inflammatory Bowel Diseases/complications
• Inpatients

• Crohn's disease
• Mediterranean diet
• gut microbiota
• inflammatory bowel diseases
• ulcerative colitis

• Biomarkers
• C-Reactive Protein/analysis
• Colitis, Ulcerative/diagnosis
• Crohn Disease/diagnosis
• Humans
• Inflammatory Bowel Diseases/diagnosis

• fruits
• gut microbiota
• inflammatory bowel disease
• juices
• lyophilized powder

Inflammatory bowel disease, encompassing Crohn’s disease (CD) and ulcerative colitis, are chronic immune-mediated inflammatory bowel diseases (IBD) that primarily affect the gastrointestinal tract with periods of activity and remission. Large body of evidence exist to strengthen the prognostic role of endoscopic evaluation for both disease activity and severity and it remains the gold standard for the assessment of mucosal healing. Mucosal healing has been associated with improved clinical outcomes with prolonged remission, decreased hospitalization, IBD-related surgeries and colorectal cancer risk. Therefore, endoscopic objectives in IBD have been incorporated as part of standard care. With the known increased risk of colorectal cancer in IBD, although prevention strategies continue to develop, regular surveillance for early detection of neoplasia continue to be paramount in IBD patients’ care. It is thanks to evolving technology and visualization techniques that surveillance strategies are continuously advancing. Therapeutic endoscopic options in IBD have also been expanding, from surgery sparing therapies such as balloon dilation of fibrostenotic strictures in CD to endoscopic mucosal resection of neoplastic lesions. In this review article, we discuss the current evidence on the use of endoscopy as part of standard of care of IBD, its role in surveillance of neoplasia, and the role of interventional endoscopic therapies.

• Inflammatory bowel disease
• Endoscopy
• Crohn’s disease
• Ulcerative colitis
• Therapeutic endoscopy
• Surveillance

• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/therapy
• Constriction, Pathologic
• Crohn Disease/diagnosis
• Crohn Disease/therapy
• Endoscopy
• Humans
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/therapy

Infection with Histoplasma capsulatum can lead to a disseminated disease involving the gastrointestinal tract presenting as diffuse abdominal pain and inflammatory diarrhea which may mimic inflammatory bowel disease (IBD).

In the current report, we discuss the case of a 41-year old male who presented to the emergency department with complaints of high-grade intermittent fevers and severe abdominal pain with associated diarrhea and hematochezia. Laboratory results demonstrated transaminitis and elevated erythrocyte sedimentation rate, C-reactive protein and ferritin levels. The patient’s presentation was thought to be an exacerbation of his underlying IBD, but further investigations revealed a positive Histoplasma antigen in the urine. The patient was offered a colonoscopy and biopsy to confirm the diagnosis; however, he refused. He was treated with itraconazole and showed significant improvement of his symptoms, thereby confirming the diagnosis of gastrointestinal histoplasmosis.

Here within, we provide a review of IBD, evaluation of chronic diarrhea, and gastrointestinal histoplasmosis.

• Histoplasmosis
• Inflammatory bowel disease
• Intestine
• Endoscopy
• Gastroenterology
• Case report

• forecasting
• inflammatory bowel disease
• predictive modeling
• prevalence

Inflammatory bowel disease (IBD) is a chronic relapsing-remitting condition affecting 600 000 people in the UK. Traditionally, patients attend outpatient clinics for monitoring regardless of their symptoms or risk of developing complications. This can lead to a mismatch between need and access: patients in remission given elective appointments displace those in need of urgent specialist attention. Novel initiatives implemented in the UK to improve outpatient monitoring have often required a well-maintained patient registry, empowered patients and significant information technology support.

In this large-scale quality improvement project at St Mark’s Hospital, a tertiary centre for IBD, we stratified over 1000 patients attending three non-complex IBD clinics over 12 months according to disease activity and risk profile. The aim was to offer a choice and subsequently transfer 50% of eligible patients to specialist nurse-led telephone clinics and demonstrate non-inferior satisfaction levels to existing outpatient follow-up. We also sought to ensure there was timely access to a newly established rapid access clinic for patients requiring urgent specialist attention.

A core project team consisting of healthcare professionals, patients and quality improvement scientists met regularly. The team tested and scaled up interventions using ‘Plan-Do-Study-Act’ cycles within the ‘Model for Improvement’ framework and analysed data continuously using statistical process charts.

Over 12 months, the average number of eligible patients transferred to telephone clinics rose from 17.6% (42/239) using a questionnaire method to 59.3% (73/123) using active discussion in clinic. Patient satisfaction scores remained high and non-inferior to baseline scores in face-to-face clinics. The median waiting time to be seen in the rapid access clinic was 6.5 days.

This is the first published study to report on the successful stratification of patients with IBD based on disease activity and risk of complications to create a more responsive, sustainable and patient-centred model for IBD monitoring.

• chronic disease management
• hospital medicine
• outpatients
• patient-centred care
• quality improvement

• Administrative data
• Crohn’s disease
• Epidemiology
• Hospitalization rates
• Ulcerative colitis

• genetics
• inborn errors of immunity
• inflammatory bowel disease
• pathomechanisms

• Animals
• Gene-Environment Interaction
• Homeostasis
• Humans
• Immunity/genetics
• Inflammation/genetics
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/immunology
• Phenotype

• I 2250 Austrian Science Fund FWF

• Colitis, ulcerative
• Compliance
• Crohn disease
• Drug
• Inflammatory bowel diseases

Little information is available of markers that assess the disease course in dogs with idiopathic inflammatory bowel disease (IBD).

Evaluate relationship between disease severity and serum and fecal biomarkers in dogs with idiopathic IBD before and after treatment.

Sixteen dogs with idioptahic IBD and 13 healthy dogs.

Prospective case control study. Canine IBD activity index (CIBDAI) clinical score, serum concentrations of C‐reactive protein (CRP), perinuclear antineutrophil cytoplasmic antibodies (pANCA), and serum and fecal canine calprotectin (cCP) were measured before and after 21 days of treatment.

Serum CRP (median 3.5 mg/L; range: 0.1‐52.4 mg/L), fecal cCP (median 92.3 μg/g; range: 0.03‐637.5 μg/g), and CIBDAI scores significantly increased in dogs with IBD before treatment compared with serum CRP (median 0.2 mg/L; range: 0.1‐11.8 mg/L; P < .001), fecal cCP (median 0.67 μg/g; range: 0.03‐27.9 μg/g; P < .001) and CIBDAI (P < .001) after treatment. No significant associations between CIBDAI scores and before or after treatment serum biomarkers. There was a significant association between fecal cCP and CIBDAI scores before treatment (rho = 0.60, P = .01). CRP and fecal cCP significantly decreased after treatment (median 3.5 mg/L v. 0.2 mg/L; P < .001 and 92.3 μg/g v. 0.67 μg/g; P = .001, respectively).

Our data indicate that measurement of fecal cCP concentration is a useful biomarker for noninvasive evaluation of intestinal inflammation. Dogs with severe signs of GI disease more often have abnormal markers than dogs having less severe disease.

• biomarkers
• diarrhea and vomiting
• dogs
• inflammation

• Biomarkers
• Crohn’s
• calprotectin
• colitis
• inflammatory bowel disease

• Crohn’s disease
• fatigue
• inflammatory bowel disease
• ulcerative colitis

• Enteric nervous system
• Gut motility
• Host–microbe interactions
• Inflammatory bowel disease
• Intestinal epithelial cell
• Microbiota

• Biomarker
• Fecal calprotectin
• Inflammatory bowel disease
• Mucosal healing

• Biomarkers/analysis
• Feces/chemistry
• Humans
• Inflammation/diagnosis
• Inflammation/pathology
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/physiopathology
• Intestinal Mucosa/pathology
• Leukocyte L1 Antigen Complex/analysis
• Predictive Value of Tests
• Recurrence
• Reproducibility of Results

• Canadian Institutes of Health Research

Ulcerative colitis (UC) is an inflammatory bowel disease, and its pathogenesis includes genetic, environmental, and immunological factors, such as T helper cells and their secreted cytokines. T helper cells are classified as Th1, Th2, and Th17 cells. However, it is unclear which T helper cells are important in UC. Dextran sulfate sodium (DSS)-induced colitis is a commonly used model of UC. In this study, we induced DSS colitis in Th1 dominant (T-bet transgenic (Tg)) mice, Th2 dominant (GATA-3 Tg) mice, and Th17 dominant (RORγt Tg) mice to elucidate the roles of T helper cell in DSS colitis. The results showed that GATA-3 Tg mice developed the most severe DSS colitis compared with the other groups. GATA-3 Tg mice showed a significant decreased in weight from day 1 to day 7, and an increased high score for the disease activity index compared with the other groups. Furthermore, GATA-3 Tg mice developed many ulcers in the colon, and many neutrophils and macrophages were detected on day 4 after DSS treatment. Measurement of GATA-3-induced cytokines demonstrated that IL-13 was highly expressed in the colon from DSS-induced GATA-3 Tg mice. In conclusion, GATA-3 overexpression in T-cells and IL-13 might play important roles in the development of DSS colitis.

Unambiguous diagnosis of the two main forms of inflammatory bowel diseases (IBD): Ulcerative colitis (UC) and Crohn’s disease (CD), represents a challenge in the early stages of the diseases. The diagnosis may be established several years after the debut of symptoms. Hence, protein biomarkers for early and accurate diagnostic could help clinicians improve treatment of the individual patients. Moreover, the biomarkers could aid physicians to predict disease courses and in this way, identify patients in need of intensive treatment. Patients with low risk of disease flares may avoid treatment with medications with the concomitant risk of adverse events. In addition, identification of disease and course specific biomarker profiles can be used to identify biological pathways involved in the disease development and treatment. Knowledge of disease mechanisms in general can lead to improved future development of preventive and treatment strategies. Thus, the clinical use of a panel of biomarkers represents a diagnostic and prognostic tool of potentially great value. The technological development in recent years within proteomic research (determination and quantification of the complete protein content) has made the discovery of novel biomarkers feasible. Several IBD-associated protein biomarkers are known, but none have been successfully implemented in daily use to distinguish CD and UC patients. The intestinal tissue remains an obvious place to search for novel biomarkers, which blood, urine or stool later can be screened for. When considering the protein complexity encountered in intestinal biopsy-samples and the recent development within the field of mass spectrometry driven quantitative proteomics, a more thorough and accurate biomarker discovery endeavor could today be performed than ever before. In this review, we report the current status of the proteomics IBD biomarkers and discuss various emerging proteomic strategies for identifying and characterizing novel biomarkers, as well as suggesting future targets for analysis.

• Inflammatory bowel disease
• Biomarker
• Proteomics
• Citrullination
• Ulcerative colitis
• Crohn’s disease
• Posttranslational modification

• Apoptosis
• Biomarkers/blood
• Biomarkers/metabolism
• Citrulline/chemistry
• Colitis, Ulcerative/blood
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/metabolism
• Crohn Disease/blood
• Crohn Disease/diagnosis
• Crohn Disease/metabolism
• Feces
• Humans
• Inflammatory Bowel Diseases/blood
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/metabolism
• Mass Spectrometry
• Protein Processing, Post-Translational
• Proteomics/methods
• Treatment Outcome

Many patients with inflammatory bowel disease (IBD) often complain of fatigue. To date, only a few studies in Western countries have focused on fatigue related to IBD, and fatigue has never been specifically studied in Asian IBD patients. The aim of the present study was to investigate the fatigue level and fatigue-related factors among Korean IBD patients.

Patients in remission or with mild to moderate IBD were included. Fatigue was assessed using the Functional Assessment of Chronic Illness Therapy-Fatigue and the Brief Fatigue Inventory. Corresponding healthy controls (HCs) also completed both fatigue questionnaires.

Sixty patients with Crohn disease and 68 patients with ulcerative colitis (UC) were eligible for analysis. The comparison group consisted of 92 HCs. Compared with the HCs, both IBD groups were associated with greater levels of fatigue (p<0.001). Factors influencing the fatigue score in UC patients included anemia and a high erythrocyte sedimentation rate (ESR).

Greater levels of fatigue were detected in Korean IBD patients compared with HCs. Anemia and ESR were determinants of fatigue in UC patients. Physicians need to be aware of fatigue as one of the important symptoms of IBD to better understand the impact of fatigue on health-related quality of life.

• Colitis, ulcerative
• Crohn disease
• Fatigue
• Inflammatory bowel diseases

• 8-Hydroxy-2'-Deoxyguanosine
• Animals
• Azoxymethane
• Carcinogenesis/chemically induced
• Carcinogenesis/genetics
• Carcinogenesis/immunology
• Carcinogenesis/metabolism
• Colitis/chemically induced
• Colitis/genetics
• Colitis/immunology
• Colitis/metabolism
• Colonic Neoplasms/chemically induced
• Colonic Neoplasms/genetics
• Colonic Neoplasms/immunology
• Colonic Neoplasms/metabolism
• DNA Damage
• Deoxyguanosine/analogs & derivatives
• Deoxyguanosine/chemistry
• Dextran Sulfate
• Diet
• Epidermal Growth Factor/genetics
• Epidermal Growth Factor/immunology
• Gene Expression Regulation
• Inflammation/chemically induced
• Inflammation/genetics
• Inflammation/immunology
• Inflammation/metabolism
• Mice
• Mice, Inbred C57BL
• Selenium/deficiency
• Signal Transduction
• Transforming Growth Factor beta/genetics
• Transforming Growth Factor beta/immunology
• Weight Loss

• P01CA116087 NCI NIH HHS
• P50CA095103 NCI NIH HHS
• P50 CA095103 NCI NIH HHS
• R25 GM062459 NIGMS NIH HHS
• P01 CA116087 NCI NIH HHS
• P30CA068485 NCI NIH HHS
• R01DK053620 NIDDK NIH HHS
• P01CA028842 NCI NIH HHS
• T32CA009592-26 NCI NIH HHS
• P01 CA028842 NCI NIH HHS
• R01 DK053620 NIDDK NIH HHS
• 1F31CA167920 NCI NIH HHS
• R01 CA190612 NCI NIH HHS
• R01AT004821 NCCIH NIH HHS
• P30 DK058404 NIDDK NIH HHS
• DK080221 NIDDK NIH HHS
• R01 AT004821 NCCIH NIH HHS
• R01AT004821-S1 NCCIH NIH HHS
• R01DK82813 NIDDK NIH HHS
• K08 DK080221 NIDDK NIH HHS
• R01 DK082813 NIDDK NIH HHS
• T32 GM007347 NIGMS NIH HHS
• I01 BX001453 BLRD VA
• P30 CA068485 NCI NIH HHS
• I01 BX001426 BLRD VA
• T32 CA009592 NCI NIH HHS
• F31 CA167920 NCI NIH HHS
• F30 DK096718 NIDDK NIH HHS

Incidence and prevalence of ulcerative colitis follow a north–south (latitudinal) gradient and increases northwards at the northern hemisphere or southwards at the southern hemisphere. The disease has increased during the last decades. The temporal trend has been explained by the hygiene hypothesis, but few parallel explanations exist for the spatial variability. Many factors are linked to latitude such as climate. Our purpose was to investigate the association between variables governing the climate and prospectively identified patients.

In this study, we used a subset of the population-based Cohort of Norway (n = 80412) where 370 prevalent cases of ulcerative colitis were identified through self-reported medication. The meteorological and climatic variables temperature, precipitation, and altitude were recorded from weather stations of the Norwegian Meteorological Institute. Summer temperature was used to capture environmental temperature.

Summer temperature was significantly related to the prevalence of ulcerative colitis. For each one-degree increase in temperature the odds for ulcerative colitis decreased with about 9% (95% CI: 3%-15%). None of the other climatic factors were significantly associated to the risk of ulcerative colitis. Contextual variables did not change the association to the prevalence of ulcerative colitis.

The present results show that the prevalence of ulcerative colitis is associated to summer temperature. Our speculation is that summer temperature works as an instrumental variable for the effect of microbial species richness on the development of ulcerative colitis. Environmental temperature is one of the main forces governing microbial species richness and the microbial composition of the commensal gut flora is known to be an important part in the process leading to ulcerative colitis.

Inflammatory bowel diseases (IBDs) are diseases that occur primarily in adolescence and early adult life. A second peak of IBD incidence occurs at the age of 50–80 years, while reports of first diagnosis after the age of 80 years are extremely rare. It is difficult to establish the true incidence of IBD in older patients due to problems of case definition, population, and particularly because it may be confused with other clinical conditions. A 91-year-old man was admitted to the Emergency Department with progressively worsening abdominal pain and 2–4 episodes of bloody diarrhea daily for the last month. Similar symptoms were not reported by the patient or his family during the past. Complete blood count and biochemical tests were normal, while stool examination showed erythrocytes and white blood cells. Pelvic CT showed inflammatory changes and loss of homogeneity in the perirectal fat together with considerable bowel wall thickening of both the rectum and sigmoid. Colonoscopy revealed edema, hyperemia and spontaneous friability, as well as microulcerations of the rectosigmoid mucosa. Tissue biopsies revealed histopathological lesions compatible with IBD. Finally the patient was treated with metronidazole, ciprofloxacin and mesalazine, with clear clinical improvement during the 5th day of treatment, and was finally discharged with almost normal stools. In conclusion, we report the case of first diagnosis of IBD in a 91-year-old man. The prevalence of IBD in patients aged >80 years is difficult to determine. Diagnostic tools are the same as for other age groups, but diagnosis may be difficult because there are a number of clinical conditions that may mimic IBD at this age. The treatment options are those used in younger patients, but special precautions should be taken.

• Bloody diarrhea
• Crohn's disease
• Elderly
• Inflammatory bowel disease
• Ulcerative colitis

Anatomical progression of pediatric inflammatory bowel disease is under-reported. The aim of this work was to examine possible changes in the anatomical distribution of IBD in pediatric patients at diagnosis and at follow up.

In a retrospective cohort study, the medical records of children with inflammatory bowel disease were examined. Patients who had at least 2 endoscopic/colonoscopic examinations were included. Primary outcome was histopathological progression based on histopathological examination of biopsies taken during endoscopic and colonoscopic bowel examination. Factors predictive of disease progression were also examined.

A total of 98 patients fulfilled inclusion criteria (49 female, 54 with ulcerative colitis, range 2 – 17 years, mean age at diagnosis was 10.6 years, SD ± 3.67), the mean duration of follow up was 32.9 months (range 0.1 – 60 months, SD ± 8.54). In the ulcerative colitis group, 41% had disease progression and none of the examined variables (age, gender, laboratory markers, growth and disease activity at diagnosis) appeared to effect disease progression. In the Crohn’s disease group, 75% had disease progression. Girls (OR = 0.13, 95% CI 0.02 – 0.79) and patients with high erythrocytic sedimentation rate (OR=0.942, 95% CI 0.894 – 0.99) were predictive for disease progression.

Despite maximum therapy, the majority of children with Crohn’s disease appeared to have histopathological disease progression. Female sex and high erythrocytic sedimentation rate seemed to be predictive for disease progression. None of the factors analyzed seemed predictive of disease progression in ulcerative colitis.

Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), are chronic, progressive and disabling disorders. Over the last few decades, new therapeutic approaches have been introduced which have led not only to a reduction in the mortality rate but also offered the possibility of a favorable modification in the natural history of IBD. The identification of clinical, genetic and serological prognostic factors has permitted a better stratification of the disease, thus allowing the opportunity to indicate the most appropriate therapy. Early treatment with immunosuppressive drugs and biologics has offered the opportunity to change, at least in the short term, the course of the disease by reducing, in a subset of patients with IBD, hospitalization and the need for surgery. In this review, the crucial steps in the natural history of both UC and CD will be discussed, as well as the factors that may change their clinical course. The methodological requirements for high quality studies on the course and prognosis of IBD, the true impact of environmental and dietary factors on the clinical course of IBD, the clinical, serological and genetic predictors of the IBD course (in particular, which of these are relevant and appropriate for use in clinical practice), the impact of the various forms of medical treatment on the IBD complication rate, the role of surgery for IBD in the biologic era, the true magnitude of risk of colorectal cancer associated with IBD, as well as the mortality rate related to IBD will be stressed; all topics that are extensively discussed in separate reviews included in this issue of World Journal of Gastroenterology.

• Inflammatory bowel disease
• Ulcerative colitis
• Crohn’s disease
• Natural history
• Clinical course
• Complications
• Therapy
• Surgery
• Mortality

Annexin A1 (ANXA1) inhibits NF-κB, a key regulator of inflammation, the common pathophysiological mechanism of inflammatory bowel diseases (IBD). MC-12, an ANXA1-based tripeptide, suppresses NF-κB activation. Here, we determined the efficacy of MC-12 in the control of IBD. Mice with colitis induced by dextran sodium sulfate (DSS) or 2,4,6-trinitro benzene sulfonic acid (TNBS) were treated with various doses of MC-12 administered intraperitoneally, orally or intrarectally. We determined colon length and the histological score of colitis, and assayed: in colon tissue the levels of TNF-α, IFN-γ, IL-1β, IL-6 and IL-10 by RT-PCR; prostaglandin E₂ (PGE₂), cytoplasmic phospholipase A₂ (cPLA₂) and myeloperoxidase by immunoassay; and COX-2 and NF- κB by immunohistochemistry; and in serum the levels of various cytokines by immunoassay. In both models MC-12: reversed dose-dependently colonic inflammation; inhibited by up to 47% myeloperoxidase activity; had a minimal effect on cytoplasmic phospholipase A₂; reduced significantly the induced levels of TNF-α, IFN-γ, IL-1β, IL-6 and IL-10, returning them to baseline. DSS and TNBS markedly activated NF-κB in colonic epithelial cells and MC-12 decreased this effect by 85.8% and 72.5%, respectively. MC-12 had a similar effect in cultured NCM460 normal colon epithelial cells. Finally, MC-12 suppressed the induction of COX-2 expression, the level of PGE₂ in the colon and PGE₂ metabolite in serum. In conclusion, MC-12, representing a novel class of short peptide inhibitors of NF-κB, has a strong effect against colitis in two preclinical models recapitulating features of human IBD. Its mechanism of action is complex and includes pronounced inhibition of NF-κB. MC-12 merits further development as an agent for the control of IBD.

• Adaptation, Psychological
• Adult
• Aged
• Aged, 80 and over
• Confidence Intervals
• Female
• Health Status Indicators
• Humans
• Inflammatory Bowel Diseases/psychology
• Language
• Male
• Middle Aged
• Norway
• Psychometrics
• Quality of Life/psychology
• Regression Analysis
• Reproducibility of Results
• Stress, Psychological
• Surveys and Questionnaires/standards
• Translating
• Young Adult

• Appendicectomy
• Dextrin sulfate sodium
• Murine colitis
• Oral tolerance
• Th1-Th2 balance

• Administration, Oral
• Animals
• Appendectomy/adverse effects
• Colitis/chemically induced
• Colitis/immunology
• Colitis/prevention & control
• Colitis/therapy
• Colon/drug effects
• Colon/immunology
• Colon/metabolism
• Colon/pathology
• Dextran Sulfate/adverse effects
• Disease Models, Animal
• Hypersensitivity, Delayed/chemically induced
• Hypersensitivity, Delayed/immunology
• Hypersensitivity, Delayed/therapy
• Immune Tolerance
• Injections, Subcutaneous
• Intestinal Mucosa/immunology
• Male
• Mice
• Mice, Inbred BALB C
• Ovalbumin/administration & dosage
• Ovalbumin/pharmacology
• Peyer's Patches/drug effects
• Peyer's Patches/pathology
• Proteins/administration & dosage
• Proteins/immunology
• Proteins/therapeutic use
• Serum Albumin, Bovine/pharmacology
• Th1 Cells/drug effects
• Th1 Cells/pathology
• Th2 Cells/drug effects
• Th2 Cells/pathology

• Genetic Predisposition to Disease
• Genetics, Population/methods
• Human Genome Project/organization & administration
• Humans
• Inflammatory Bowel Diseases/epidemiology
• Inflammatory Bowel Diseases/genetics
• Phenotype

• G0600329 Medical Research Council
• G0800759 Medical Research Council
• G0800675 Medical Research Council

• Animals
• Bone Resorption/complications
• Bone Resorption/epidemiology
• Bone Resorption/metabolism
• Bone Resorption/therapy
• Bone and Bones/metabolism
• Celiac Disease/complications
• Celiac Disease/epidemiology
• Celiac Disease/metabolism
• Celiac Disease/therapy
• Humans
• Inflammation/complications
• Inflammation/metabolism
• Inflammation/pathology
• Inflammation/physiopathology
• Inflammatory Bowel Diseases/complications
• Inflammatory Bowel Diseases/epidemiology
• Inflammatory Bowel Diseases/metabolism
• Inflammatory Bowel Diseases/therapy
• Osteoporosis/complications
• Osteoporosis/epidemiology
• Osteoporosis/metabolism
• Osteoporosis/therapy