Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intestinal Inflammation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,387 records · Page 77Linked to original sources
PubMed2002

The leptin defense against wasting is abolished in the IL-2-deficient mouse model of inflammatory bowel disease.

Anorexia is a major complication of inflammatory bowel disease (IBD). We postulated that chronic intestinal inflammation with increased proinflammatory cytokines elevates serum leptin concentration, thereby contributing to anorexia. This hypothesis was studied in interleukin-2-deficient (IL-2(-/-)) mice, a model of IBD with elevated proinflammatory cytokine production. IL-2(-/-), wild-type pair-fed and wild-type control male mice (8 wk old) were fed regular laboratory mouse food for 2 wk. The IL-2(-/-) and pair-fed groups consumed less food and lost weight. Serum leptin concentrations in the IL-2(-/-) mice in the fed state were lower than controls, but not different from pair-fed mice, and paradoxically increased in the starved state to levels significantly higher than both starved control and pair-fed groups. This result did not change when serum leptin was adjusted for amount of body fat. These data show abnormal leptin responses in IL-2(-/-) mice with increased leptin concentrations disproportionate to fat mass and prevention of the normal decline in leptin with food restriction.

Animals↗
PubMed2003

Molting and Salmonella enterica serovar enteritidis infection: the problem and some solutions.

Induced molting is an important economic tool used by the egg industry to recycle an aging layer flock. It is estimated that approximately 70% of the flocks nationwide and almost 100% in California are molted annually. Considering that there are approximately 240 million hens in production in the U.S., a rough estimate of the numbers of hens molted every year would be between 144 and 168 million birds, a substantial number. There are many methods to induce molt, but feed removal until hens lose a specific weight is the most prevalent molt strategy in the U.S. However, experimental studies in our laboratory have shown that induced molting via feed removal depresses the immune system of hens and exacerbates a Salmonella enteritidis (SE) problem in a simulated flock situation. Molted hens excreted significantly higher SE numbers in the feces, had higher numbers of SE in internal organs, and exhibited more intestinal inflammation. Molted hens were 100- to 1,000-fold more susceptible to infection by SE and therefore more readily transmitted the organism to uninfected hens in neighboring cages. With the problems identified, solutions were sought, and several were successful in ameliorating the SE issue. Antibiotic therapy, vaccination, and use of low-energy, low-calcium diets to molt hens all dramatically decreased SE shedding during molt. All of the solutions provide the producer with many potential solutions to the SE food safety issue and still allow them to recycle their hens.

Animal Feed↗
PubMed1993

Ileal pouch arthritis.

The association between arthritis and intestinal inflammation is well established, but the pathogenesis of the inflammatory joint disease remains speculative. We report six patients who developed a polyarthritis following restorative proctocolectomy with an ileal pouch-anal anastomosis (IPAA) for extensive ulcerative colitis between 1983 and 1990. Six patients were identified with no complaint of joint symptoms before surgery. The average time to onset of arthritis following surgery was 8 months (1 week-yr). The typical features were of an acute symmetrical polyarthritis involving the peripheral and axial skeleton. Early morning stiffness was pronounced in two and minimal in the rest. Three patients were treated with a course of prednisolone and remain in remission (1-4 yr). We believe that this is a novel form of arthritis clearly linked to pouch surgery which may provide important clues to the role of gastrointestinal antigens in rheumatic diseases.

Adult↗
PubMed2000

Comparative studies of the colonic in situ expression of intercellular adhesion molecules (ICAM-1, -2, and -3), beta2 integrins (LFA-1, Mac-1, and p150,95), and PECAM-1 in ulcerative colitis and Crohn's disease.

A dysregulated local immune defense with a constant influx of leukocytes provides a basis for continuous intestinal inflammation in ulcerative colitis (UC) and Crohn's disease (CD). Cell adhesion molecules are pivotal for the migration of leukocytes from the circulation toward the colonic epithelium. A study quantifying the cells expressing intercellular adhesion molecules (ICAMs), beta2 integrins, and platelet-endothelial cell adhesion molecule-1 (PECAM-1) in the colon was performed to illustrate the leukocyte migration pathway in inflammatory bowel disease. Serial colonic sections (10 UC, 10 CD, and 10 controls) were stained immunohistochemically for ICAM-1, ICAM-2, ICAM-3, CD11a, CD11b, CD18, and PECAM-1. Cell adhesion molecule expression was evaluated quantitatively with reference to topographic localization. In UC, polymorphonuclear leukocytes (PMNs) in contact with the crypt epithelium and in crypt abscesses expressed CD11b. CD tissue was characterized by CD11a-, CD11c-, and ICAM-1-expressing cells. ICAM-1 was detected on endothelial cells, leukocytes, and apical parts of epithelial membranes, whereas ICAM-2 was expressed on basal epithelial membranes. Most infiltrating leukocytes expressed ICAM-3, whereas perivascular mononuclear cells expressed PECAM-1. Interestingly, the epithelial basement membrane in UC stained for CD18. In conclusion, CD11b, CD18, and ICAM-2 seem to be important for PMN transepithelial migration in UC, whereas CD11a, CD11c, ICAM-1, and ICAM-3 seem central in leukocyte locomotion and aggregation in CD. Differentiated upregulation of cell adhesion molecules is suggested to be essential for the diversities between UC and CD.

CD18 Antigens↗
PubMed2000

Small intestinal permeability.

The noninvasive assessment of small intestinal permeability in humans is now within the capability of any routine biochemistry laboratory. There remain however, many pitfalls for the unwary when performing these tests. Importantly, it has now been shown that normal intestinal permeability relates to geographical location rather than race. Recent studies show that it may be possible to simplify the procedure even further. The main recent focus of interest in measuring intestinal permeability relates to patients with AIDS and inflammatory bowel disease, the effects of nonsteroidal anti-inflammatory drugs on the small bowel, and the use of these tests in the pediatric population and critically ill. Some groups have now started to focus their attention on the possible systemic consequences of increased intestinal permeability, whereas others have shown that increased small bowel permeability results in small intestinal inflammation that may in turn be associated with blood and protein loss.

Journal Article↗
PubMed2000

Genomics and inflammatory bowel disease.

Genomic technologies offer new approaches to the investigation of etiology and pathophysiology of inflammatory bowel disease (IBD). Several areas of application for these new technologies are possible. One such application is the search for gene variations predisposing to the development of the disorder in multiply-affected families. Genome-wide linkage studies have defined replicated susceptibility regions for IBD on chromosomes 6, 12, and 16. These susceptibility regions are still very large and each contain several hundred positional candidate genes. Efforts are under way at several centers to define the underlying molecular variants using systematic linkage disequilibrium and candidate gene methods. The pharmacogenetic investigation of gene variations may predict response to certain medications to target these therapeutic interventions more precisely. The use of global gene expression technologies may allow the identification of new pathways or molecules in the inflammatory process. This seems to be especially relevant because currently only approximately 8,000 of the estimated 100,000 human genes are characterized. In summary, genomic methodologies will profoundly influence the progress of IBD research and may lead to novel insights into both etiology and pathophysiology of chronic intestinal inflammation.

Journal Article↗
PubMed2003

Mucosal T cells: mediators or guardians of inflammatory bowel disease?

Because the mucosal immune system is continuously exposed to a myriad of potentially harmful environmental antigens, it frequently reacts with antiinflammatory/regulatory T cell responses driven by TGF-beta-producing TH3 cells and IL-10-producing regulatory T cells. Intestinal inflammation in patients with inflammatory bowel diseases is thought to result from an overwhelming uncontrolled activation of the mucosal immune system induced by antigens of the normal luminal flora in genetically susceptible individuals. Inflammatory bowel disease appears to be mediated by subsets of CD4 T lymphocytes or NK T cells secreting high levels of proinflammatory cytokines such as TNF-alpha. The increased expression of integrins/addressins in the inflamed gut and the increased expression of adhesion molecules on T cells facilitate migration of these pathogenic T cell subsets into the lamina propria. Additionally, the local activation of antiapoptotic pathways in pathogenic T lymphocytes leads to a further accumulation of these cells in the lamina propria, causing perpetuation and chronicity of inflammatory bowel disease. This concept is underlined by the finding that most potent immunosuppressive drugs used in treatment of inflammatory bowel disease seem to work by inducing T cell apoptosis via inhibition of STAT-3 and NFkappaB-dependent antiapoptotic pathways. Taken together, distinct T cell subsets appear to act as mediators or guardians of inflammatory bowel disease, and thus they play a central role in controlling the delicate balance between proinflammatory and antiinflammatory immune responses in the gut.

Journal Article↗
PubMed2004

Biomarkers in inflammatory bowel disease.

PURPOSE OF REVIEW: Inflammatory bowel disease is characterized by chronic intestinal inflammation in the absence of a recognized pathogen. In its classic description, there are two principal forms of inflammatory bowel disease: Crohn disease and ulcerative colitis. The clinical heterogeneity of these disorders alludes to the possibility of diverse pathogenetic mechanisms underlying inflammatory bowel diseases. The purpose of this review is to summarize the latest information on biomarkers of Crohn disease and ulcerative colitis. RECENT FINDINGS: The authors have focused on serologic markers for which emerging data support their use as predictors of disease evolution. Serologic markers such as perinuclear antineutrophil cytoplasmic antibody, anti-Saccharomyces cerevisiae antibody, anti-OmpC, and anti-I2 may be useful in distinguishing inflammatory bowel diseases from functional disorders and ulcerative colitis from Crohn disease and predicting complications of disease. Genetic markers such as CARD15/NOD2 may be useful in the future when combined with other markers to predict disease course. Biochemical markers of inflammation such as C-reactive protein are useful to stratify patients likely to respond to biologic therapies and to follow response to treatment. In the future, functional genomics and proteomics will be used to rapidly screen patients for subclinical characteristics that can predict disease course and response to therapy. SUMMARY: A variety of biomarkers can be used to stratify patients with inflammatory bowel disease into more homogeneous subgroups with respect to response to therapy and disease progression.

Journal Article↗
PubMed1996

Immune-related systemic manifestations of inflammatory bowel disease. A prospective study of 792 patients.

The prevalence of immune-related systemic manifestations associated with inflammatory bowel disease varies widely in different studies. This prospective hospital study examines the prevalence and clinical aspects of these manifestations. A total of 792 patients, 449 with Crohn's disease and 343 with ulcerative colitis, were followed up from diagnosis to 20 years. Data related to systemic manifestations and to the extent and severity of intestinal lesions were obtained at diagnosis and during follow-up. Extraintestinal manifestations related to the activity of intestinal inflammation appeared at least once in 25.8% of the patients. The cumulative probability of extraintestinal manifestations increased from 12%-30% during the 20-year follow-up; it was significantly higher in patients with Crohn's disease (p < 0.01). Arthritis (p < 0.001) and erythema nodosum (p < 0.01) were more frequent in Crohn's disease. A significant positive association of arthritis with skin, eye, and mouth complications was observed (p < 0.001). Bowel-related systemic manifestations appeared frequently together in the same patient (p < 0.001). Patients with any of these manifestations ran a higher risk of developing another one. Autoimmune manifestations were associated with both Crohn's disease and ulcerative colitis.

Adult↗
PubMed2003

Use of probiotics in the treatment of inflammatory bowel disease.

The gut flora plays a fundamental role in maintaining normal intestinal function. A disturbance of this flora, or the host response to this flora, has been clearly demonstrated to play a role in the pathogenesis of inflammatory bowel disease (IBD). This has led to attempts to modify the bacterial flora with "live non-pathogenic organisms that confer health benefits by improving the microbial balance," otherwise known as probiotics. Recent attention has focused on this potential strategy to treat or prevent IBD. The potential therapeutic benefit is enhanced by the natural and apparently safe approach that probiotics offer. Animal models of colitis have provided the proof of principle that probiotics can prevent and treat established intestinal inflammation. Controlled clinical studies have demonstrated the efficacy of probiotics in the maintenance of remission of pouchitis, prophylaxis of pouchitis after the formation of an ileoanal reservoir, maintenance of remission of ulcerative colitis, and treatment of Crohn's disease. However, large controlled trials are needed to definitively establish the place for probiotics in the treatment of IBD and resolve issues such as the dose, duration, frequency of treatment, and use of single or multiple strains. Research is focusing on establishing the mechanism of action, so that treatments with individually tailored properties are developed and innovative approaches are explored.

Animals↗
PubMed2006

Extraintestinal manifestations of inflammatory bowel diseases.

Inflammatory bowel diseases are associated with extraintestinal manifestations involving almost every organ system in the body. They occur in approximately 20% to 40% of patients with inflammatory bowel diseases. Immune-related and genetic mechanisms play an important role in the pathogenesis of these complications. Peripheral arthritis, erythema nodosum, and episcleritis respond to the treatment of the underlying intestinal inflammation, whereas axial arthropathy, pyoderma gangrenosum, and uveitis do not. Immunomodulator therapy, particularly with biologic agents has been shown to be effective in treating some of the extraintestinal manifestations. Early recognition and treatment are crucial in preventing major morbidity.

Autoimmunity↗
PubMed1990

Cyclosporin-responsive enteropathy and protracted diarrhea.

We describe a child born to unrelated parents who developed severe protracted secretory type diarrhea associated with subtotal villus atrophy and intestinal inflammation at the age of 19 months. No infectious, metabolic, or anatomical basis for this condition was identified and the child required total parenteral nutrition for a period of 18 months despite trials of special enteral formulas, steroids, and anti-inflammatory agents. This refractory "enteropathy" responded dramatically to the introduction of cyclosporin, with cessation of the secretory diarrhea, recovery from the enteropathy, and cessation of parenteral nutrition. The symptoms relapsed when cyclosporin was briefly discontinued and improved following reintroduction of this drug. This experience suggests a role for immune factors in the pathogenesis of the enteropathy in this case and that a trial of cyclosporin is worthy of consideration in similar cases.

Cyclosporins↗
PubMed2004

Gluten-free diet has a beneficial effect on chromosome instability in lymphocytes of children with coeliac disease.

OBJECTIVES: Children with coeliac disease (CD) have an increased number of chromosome aberrations in peripheral blood lymphocytes. Whether genetically determined or a secondary phenomenon in CD, chromosome abnormalities may be involved in the predisposition to cancer in CD patients. The aim of the study was to follow a group of children with CD in whom the initial frequency of chromosome aberrations at diagnosis was known and to measure the same variable after a minimum of 2 years on a gluten-free diet. METHODS: Chromosome aberrations in peripheral blood lymphocytes were determined in 17 patients with CD, before and after at least 24 months of a gluten free diet (mean, 33 months), and in 15 healthy children. The differences in the frequency of aberrations were analyzed by Mann-Whitney U test and Wilcoxon matched-pairs signed-ranks test. RESULTS: Twelve patients adhered to the diet and had a significantly lower frequency of chromosome aberrations than did 5 patients not following the diet (0.16% v 1.2%; P = 0.03), whereas at presentation there had been no difference (1.54% v 1.2%; P = 0.09). The frequency of aberrations at follow-up in patients who were diet adherent was significantly lower than at presentation (1.54% v 0.16%; P = 0.02) and remained unchanged in patients who were not diet adherent (1.2% v 1.2%; P = 1). After at least 24 months of a gluten-free diet, children with CD did not differ from healthy control subjects (0.16% v 0.27%; P = 0.54), whereas children not following the diet had an increased frequency of aberrations (1.2% v 0.27%; P = 0.05). CONCLUSIONS: The frequency of chromosome aberrations in peripheral blood lymphocytes of patients with CD decreased significantly on a gluten-free diet. We conclude that genomic instability is a secondary phenomenon, possibly caused by chronic intestinal inflammation.

Adolescent↗
PubMed1992

Monoclonal antigranulocyte antibody imaging in inflammatory bowel disease: a preliminary report.

The 99Tcm-labelled antigranulocyte antibody BW250/183 has been used in the detection of intestinal inflammation in patients with active ulcerative colitis and Crohn's disease. Planar images were obtained up to 24 h after intravenous injection of the antibody. Eight out of nine patients with ulcerative colitis and six out of seven patients with Crohn's disease gave positive images. In 11 patients distribution of the inflammation was confirmed by barium studies, colonoscopy or surgery, whilst in two the antibody scan suggested more extensive disease than barium enema. None of the patients had any adverse reactions. Imaging with BW250/183 appears to give an accurate indication of the extent of inflammation in inflammatory bowel disease.

Colitis, Ulcerative↗
PubMed2002

Diet and gastrointestinal disease.

Dietary manipulation can be an important part of therapy for several common gastrointestinal disorders. In Crohn disease, the provision of adequate protein and calories may not only improve symptoms but may be associated with acceleration of growth. In celiac disease, the dietary restriction of gluten is curative of the intestinal inflammation. In chronic nonspecific diarrhea and functional constipation, the provision of appropriate amounts of fiber and fluids may ameliorate symptoms. A thorough understanding of the role of diet is essential to the management of these disorders.

Age Factors↗
PubMed2002

Circulating soluble vascular adhesion protein 1 in patients with inflammatory bowel disease.

OBJECTIVE: A dysregulated local immune defence with a constant influx of leucocytes provides a basis for continuous intestinal inflammation in ulcerative colitis and Crohn's disease. Since vascular adhesion protein 1 (VAP-1) is one of the adhesion molecules that mediates lymphocyte binding to endothelium, we investigated the levels of soluble VAP-1 (sVAP-1) in the sera of inflammatory bowel disease (IBD) patients compared with healthy controls. METHODS: sVAP-1 serum levels were measured in 161 IBD patients (90 ulcerative colitis, 71 Crohn's disease) and 93 controls using a commercially available enzyme-linked immunosorbent assay (ELISA). sVAP-1 levels were correlated with disease activity and localization. In 42 patients, sVAP-1 levels were measured in both the active and inactive phases of the disease. RESULTS: sVAP-1 serum levels were detected in all control and IBD subjects. Mean sVAP-1 levels were 365.5 +/- 153.5 ng/ml in ulcerative colitis patients, 336.4 +/- 172.8 ng/ml in Crohn's disease patients, and 344.7 +/- 150.4 ng/ml in healthy controls. The differences between the groups were not significant. No association between disease activity or disease localization and sVAP-1 was found. CONCLUSIONS: sVAP-1 serum concentrations are not significantly different in IBD and healthy control subjects. sVAP-1 serum levels are of no value in the assessment of disease activity or severity of inflammation in patients with IBD.

Amine Oxidase (Copper-Containing)↗
PubMed2004

Association between enhanced soluble CD40 ligand and prothrombotic state in inflammatory bowel disease.

BACKGROUND: Inflammatory bowel disease is associated with an increased incidence of thromboembolic complications. The aim of this study was to investigate the role of the soluble CD40 ligand (sCD40L), which displays prothrombotic properties, in patients with ulcerative colitis (UC) and Crohn's disease (CD) in comparison with inflammatory and healthy controls. METHODS: Plasma levels of sCD40L, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin (TAT) complex and soluble P-selectin were measured in 104 inflammatory bowel disease patients (54 ulcerative colitis and 50 Crohn's disease), in 18 cases with other causes of intestinal inflammation and in 80 healthy controls using commercially available enzyme-linked immunosorbent assays. Plasma levels of sCD40L were correlated with disease activity, type, localization and treatment as well as with the measured thrombophilic parameters. RESULTS: CD patients had significantly higher sCD40L levels than both groups of controls (CD vs HC P < 0.001; CD vs non-IBD P < 0.05). UC patients had higher but not significantly different sCD40L levels compared with the controls. Both UC and CD patients with active disease had significantly higher sCD40L levels in comparison with patients with inactive disease. Plasma levels of sCD40L were correlated with platelet count (r = 0.27, P = 0.001). They also showed a correlation with prothrombin F1+2 (r = 0.16, r = 0.03) and TAT (r = 0.15, r = 0.04) as well as with P-selectin (r = 0.19, P = 0.01). CONCLUSIONS: The increased sCD40L plasma levels may represent, at least in some degree, a molecular link between inflammatory bowel disease and the procoagualant state.

Adult↗
PubMed2005

Coombs-positive autoimmune hemolytic anemia in Crohn's disease.

BACKGROUND: Anemia often occurs in patients with inflammatory bowel diseases. However, hemolytic anemia is a rare complication and is associated with Coombs-positive autoimmune disorders. There are several reports of autoimmune hemolytic anemia in patients with ulcerative colitis, whereas there are only four reports of this complication in patients with Crohn's disease. We report a case of a severe course Coombs-positive hemolytic anemia in a patient with Crohn's disease, which was refractory to medical treatment but resolved after subtotal colectomy. CASE REPORT: A 29-year-old patient was submitted to our clinic several times because of a severe course of inflammatory bowel disease and additionally a Coombs-positive autoimmune hemolytic anemia. Histology indicated severe Crohn's disease, but neither medical treatment with steroids, nor with methotrexate, cyclosporine or tumor necrosis factor-alpha antibody had been successful in resolving the intestinal inflammation and the hemolytic anemia. As colonoscopy revealed a pancolitis and dysplastic changes, even in the less inflamed areas of the colonic mucosa, subtotal colectomy was indicated. Half a year later we observed clinical and immunological signs of complete remission (no gastrointestinal symptoms, negative Coombs test). CONCLUSION: Autoimmune hemolytic anemia is a rare complication of inflammatory bowel disease and has been almost exclusively described in ulcerative colitis. The etiology is not yet completely understood. Presumably, the colon displays a role in the production of anti-erythrocyte antibodies. The therapy of choice in Crohn's associated hemolytic anemia is thought to be medical treatment with corticoid steroids. Some authors additionally prefer immunmodulators. However, in the case presented, colectomy (without splenectomy) was necessary to resolve refractory hemolysis and the severe course of Crohn's disease.

Adult↗