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At least 793 records · Page 44Linked to original sources
PubMed2000

Growth failure occurs through a decrease in insulin-like growth factor 1 which is independent of undernutrition in a rat model of colitis.

BACKGROUND: Linear growth retardation is a frequent complication of inflammatory bowel disease in children. The precise mechanisms causing growth failure are not known. AIMS: To determine the relative contribution of reduced calorie intake and inflammation to linear growth delay and to determine the effect of inflammation on the hypothalamic-pituitary-growth axis. METHODS: Linear growth was assessed in prepubertal rats with trinitrobenzenesulphonic acid (TNBS) induced colitis, in healthy free feeding controls, and in a pair-fed group (i.e. healthy animals whose daily food intake was matched to the colitic group thereby distinguishing between the effects of undernutrition and inflammation). RESULTS: Changes in length over five days in the TNBS colitis and pair-fed groups were 30% and 56%, respectively, of healthy free feeding controls. Linear growth was significantly reduced in the colitic group compared with the pair-fed group. Nutritional supplementation in the colitic group increased weight gain to control values but did not completely reverse the growth deficit. Plasma interleukin 6 (IL-6) concentrations were sixfold higher in the colitic group compared with controls. Plasma concentrations of insulin-like growth factor 1 (IGF-1) but not growth hormone (GH) were significantly lower in the colitic compared with the pair-fed group. Administration of IGF-1 to the colitic group increased plasma IGF-1 concentrations and linear growth by approximately 44-60%. CONCLUSIONS: It seems likely that approximately 30-40% of linear growth impairment in experimental colitis occurs as a direct result of the inflammatory process which is independent of undernutrition. Inflammation acts principally at the hepatocyte/IGF-1 level to impair linear growth. Optimal growth in intestinal inflammation may only be achieved by a combination of nutritional intervention and anticytokine treatment.

Animals↗
PubMed2001

Neural change in Trichinella-infected mice is MHC II independent and involves M-CSF-derived macrophages.

Intestinal inflammation due to nematode infection impairs enteric cholinergic nerve function and induces hypercontractility of intestinal muscle. Macrophages have been implicated in the neural changes, but the subpopulation and mechanism involved are unknown. We examined whether macrophages alter nerves by virtue of their ability to activate lymphocytes via major histocompatibility complex (MHC) II-restricted antigen presentation. We also attempted to evaluate the role of macrophage subsets using op/op mice deficient in macrophage colony-stimulating factor (M-CSF). ACh release from the myenteric plexus was measured in MHC II- and M-CSF-deficient (op/op) mice infected with Trichinella spiralis. F4/80-positive macrophages and interleukin-1 beta were constitutively present in op/op and op/? mice but increased only in op/? mice postinfection. After infection, a marked suppression of ACh release occurred only in infected MHC II-deficient and op/? mice. Muscle hypercontractility remained evident in infected op/? mice. Treatment with M-CSF restored macrophage number, and this was accompanied by suppression of cholinergic nerve function during infection. Thus M-CSF plays a critical role in this model by recruiting a subset of macrophages that selectively suppresses enteric neural function.

Acetylcholine↗
PubMed2003

Delayed puberty associated with inflammatory bowel disease.

Delayed puberty frequently complicates the clinical course of young patients with inflammatory bowel disease, more often in Crohn's disease than ulcerative colitis. Undernutrition has been thought to be the main reason for delayed puberty in these patients. However, puberty may be delayed despite a normal nutritional status. Observations in patients with inflammatory bowel disease and in rats with experimental colitis suggest that inflammatory mediators may have a direct adverse influence, independent of undernutrition, on the onset and progression of puberty. Serum androgens are consistently reported to be reduced in patients with delayed puberty and inflammatory bowel disease. This reduction is not necessarily secondary to a reduction in gonadotrophins as serum concentrations of gonadotrophins have been reported to be normal or even increased in some studies. Management of delayed puberty involves calorie supplements to correct undernutrition and treatment of inflammation. Observations in boys with delayed puberty and controlled studies in experimental models of intestinal inflammation suggest that testosterone therapy can accelerate puberty.

Animals↗
PubMed2002

Adherent-invasive Escherichia coli: a putative new E. coli pathotype associated with Crohn's disease.

Crohn's disease (CD) is an inflammatory bowel disease (IBD) of unknown aetiology. Genetically engineered rodent models showed that IBDs are immunologically mediated and that luminal bacteria play an essential role in the development of the inflammation. Various bacterial pathogens have been incriminated but results have been conflicting. A new pathovar of E. coli, designated adherent-invasive Escherichia coli (AIEC) may be associated with CD. AIEC strains colonize the intestinal mucosa by adhering to intestinal epithelial cells. They are also true invasive pathogens, able to invade intestinal epithelial cells via a macropinocytosis-like process, and to survive and replicate intracellularly after lysis of the endocytic vacuole. Within macrophages, AIEC strains survive and replicate extensively without inducing host cell death and induce the release of high amounts of TNFalpha. All these virulence properties designate AIEC as a possible pathogen potentially able to induce persistent intestinal inflammation, by crossing and breaching the intestinal barrier, moving to deep tissues, and continuously activating macrophages.

Bacterial Adhesion↗
PubMed2002

Markers of inflammation in the feces of infants with cow's milk allergy.

Growing evidence exists that exposure to cow's milk elicits inflammation in the gut of infants with cow's milk allergy, irrespective of symptoms. To demonstrate inflammation and increased protein leakage from the gut during a cow's milk elimination-challenge test in fecal samples of infants presenting with different symptoms suggestive of cow's milk allergy, we measured the concentrations of alpha1-antitrypsin (AT), eosinophil cationic protein (ECP), immunoglobulin (Ig) A, and cow's milk-specific IgA antibodies, in fecal samples of 208 infants with a mean age of 7 months. Prechallenge samples were collected after a mean 3-week elimination period, and post-challenge samples were obtained 4 days after starting the challenge. Fecal levels of prechallenge total IgA (p = 0.02) and post-challenge AT (p = 0.001) were higher in infants with a positive challenge. Of these infants, pre- and post-challenge levels of ECP were higher in those reacting after 24 h than in those reacting within 1 h (p = 0.006 and p = 0.045). Prechallenge levels of ECP were higher in those showing intestinal symptoms (p = 0.008), and both pre- and post-challenge levels of total IgA were higher in those with an IgE-mediated reaction to cow's milk (p = 0.04 and p = 0.008). Regardless of the challenge result, total IgA increased during the challenge (p < 0.001 for both challenge-positive and -negative infants) and was higher in those breast-fed until the challenge than in those fed formula only (p < 0.01). Hence, in infants reacting to the cow's milk challenge, higher prechallenge levels of fecal IgA indicate increased antigenic stimuli in the gut, and higher post-challenge levels of AT reflect increased protein loss as a result of intestinal inflammation. In infants with slowly evolving gastrointestinal symptoms, increased fecal ECP may help in distinguishing patients from those who tolerate cow's milk. Individual serial follow-up of fecal IgA and ECP can be used to estimate the degree of inflammation in the gut and an appropriate time for a challenge test, but are not diagnostic tools for cow's milk allergy.

Animals↗
PubMed2006

Short-chain fructooligosaccharides, in spite of being fermented in the upper part of the large intestine, have anti-inflammatory activity in the TNBS model of colitis.

Previous studies have demonstrated the anti-inflammatory effect of fructooligosaccharides (FOS) on intestinal inflammation. The aim of the present study was to elucidate whether the colonic fermentation of these carbohydrates is a pre-requisite for this anti-inflammatory activity.With this aim short chain-FOS (SC-FOS) were used for an in vitro fermentation to elucidate the time of fermentation of these compounds. For the in vivo experiments female Wistar rats were fed several diets with different sources of fibre (5 g/kg): cellulose for control rats (n = 30) or SC-FOS (n = 20) with a high content of kestose (GF(2)) for the SC-FOS group. After one month of feeding the different diets 10 rats from each group were sacrificed to analyze cecal and colonic microflora, SCFA production and pH of intestinal contents. A distal colonic inflammation was induced to other 10 rats from each group by the administration of 10 mg of TNBS dissolved in 0.25 ml of 50% ethanol (v/v). The rest of the rats from the control group (n = 10) were rendered healthy. One week after TNBS treatment rats were sacrificed and several inflammatory parameters as well as intestinal microbiota and SCFA contents were analyzed. In vitro fermentation experiments showed that SC-FOS are fermented during the first 12 h after incorporating the oligosaccharides to intestinal contents, thus suggesting a preferential fermentation of these carbohydrates in the ileum and cecum. In fact, SC-FOS increased cecal lactobacilli and bifidobacteria counts as well as SCFA production in healthy rats. In colitic rats, SC-FOS feeding caused a decrease of MPO activity, leukotriene B4 (LTB4) production and iNOS expression. This anti-inflammatory effect was evidenced macroscopically by a significant reduction in the extent of colonic damage. SC-FOS also promoted a more favorable intestinal microbiota, increasing lactobacilli and bifidobacteria counts. In conclusion, although oligosaccharides are preferentially fermented in the upper parts of the large intestine, its prebiotic effect is extended to the distal colonic segments, thus exerting a positive effect on colonic inflammation.

Animals↗
PubMed1996

Clinical uses of probiotics for stabilizing the gut mucosal barrier: successful strains and future challenges.

Probiotic bacteria are used to treat disturbed intestinal microflora and increased gut permeability which are characteristic to many intestinal disorders. Examples include children with acute rotavirus diarrhoea, subjects with food allergy, subjects with colonic disorders and patients undergoing pelvic radiotherapy and sometimes changes associated with colon cancer development. In all such disease states altered intestinal microflora, impaired gut barrier and different types of intestinal inflammation are present. Successful probiotic bacteria are able to survive gastric conditions and colonize the intestine, at least temporarily, by adhering to the intestinal epithelium. Such probiotic microorganisms appear to be promising candidates for the treatment of clinical conditions with abnormal gut microflora and altered gut mucosal barrier functions. They are also promising ingredients to future functional foods and clinical foods for specific disease states provided that basic requirements for strains and clinical studies are carefully followed.

Animals↗
PubMed1994

Alterations in the mucosal immune system in ulcerative colitis and Crohn's disease.

Emphasis is now being placed upon obtaining a better understanding of the regulatory cytokines that normally downregulate acute intestinal inflammation. These inhibitory cytokines appear to be missing or not functioning properly in patients with inflammatory bowel disease (IBD), thereby leading to perpetuation of inflammation. As we obtain an increased understanding of immune and inflammatory regulatory processes in the intestine, we will be able to devise better future therapeutic strategies for use in our IBD patients.

Colitis, Ulcerative↗
PubMed1997

Specific mediator-directed therapy for gastrointestinal diseases.

A number of inflammatory mediators--such as proinflammatory cytokines, lipid derived eicosanoids and reactive oxygen metabolites--are elevated in chronic bowel inflammation. Existing drugs for Crohn's disease and ulcerative colitis, for example aminosalicylates and corticosteroids, work at many sites in the inflammatory cascade to control disease activity. These drugs may be associated with significant side-effects and do not always control the disease. Therefore there is an impetus to develop treatments which are safer and more specific for bowel inflammation. Specific inhibitors of inflammatory mediators have recently become available and some have been shown to be effective in animal models of bowel inflammation. Although far fewer data are currently available on specific mediator-directed therapy of intestinal inflammation in humans, early clinical trials in inflammatory bowel disease have given mixed results. It remains to be determined whether or not this strategy of specific mediator inhibition is an alternative to current therapy for chronic bowel inflammation in humans.

Animals↗
PubMed2002

Increased mucosal tumour necrosis factor alpha production in Crohn's disease can be downregulated ex vivo by probiotic bacteria.

BACKGROUND AND AIMS: Tumour necrosis factor alpha (TNF-alpha) plays a key role in the pathogenesis of intestinal inflammation in Crohn's disease. The effect of bacteria on TNF-alpha release by intestinal mucosa was investigated. METHODS: Ileal specimens were obtained at surgery from 10 patients with Crohn's disease (ileal stricture) and five disease controls undergoing right hemicolectomy (caecal cancer). Mucosal explants from each specimen were cultured for 24 hours with either non-pathogenic Escherichia coli, Lactobacillus casei DN-114001, L bulgaricus LB10, or L crispatus (each study contained blank wells with no bacteria). Tissue and bacterial viability was confirmed by lactate dehydrogenase (LDH) release and culture. Concentrations of TNF-alpha were measured in supernatants and the phenotype of the intestinal lymphocytes was analysed by flow cytometry. RESULTS: Coculture of mucosa with bacteria did not modify LDH release. Release of TNF-alpha by inflamed Crohn's disease mucosa was significantly reduced by coculture with L casei or L bulgaricus; changes induced by L crispatus or E coli were not significant. The effect of L casei and L bulgaricus was not prevented by protease inhibitors. Coculture with L casei and L bulgaricus reduced the number of CD4 cells as well as TNF-alpha expression among intraepithelial lymphocytes from Crohn's disease mucosa. None of the bacteria induced changes in non-inflamed mucosa. CONCLUSIONS: Probiotics interact with immunocompetent cells using the mucosal interface and modulate locally the production of proinflammatory cytokines.

Adult↗
PubMed1989

[Chronic inflammatory bowel diseases in cats].

The aetiology of chronic idiopathic intestinal inflammation is unknown. It is characterized by a diffuse infiltration with inflammatory cells into the intestinal mucosa and sometimes submucosa. Cats with chronic intermittent vomiting and diarrhoea, later on accompanied by anorexia and weight loss, are presented. Definitive diagnosis can be obtained by intestinal biopsy only. An immune pathogenesis is suspected, which is supported by the fact, that chronic inflammatory bowel disease responds to steroid therapy.

Animals↗
PubMed1979

Small intestine cutaneous fistulas.

A retrospective study of 174 patients with small intestine cutaneous fistulas was carried out. Cause, location of fistula, amount of output, presence of inflammation, intestinal obstruction, presence of malnutrition and anemia are associated wih an increased mortality. The results of various modes of treatment indicate that intestinal resection with primary anastomosis, carried out six weeks or later after the onset of the fistula, was associated with the lowest mortality and the highest success rate.

Fistula↗
PubMed1984

[Immunomorphological evaluation of intestinal function in periodic disease patients].

Based on clinico-endoscopic, x-ray, immunological and immunohistochemical studies the authors demonstrate the role of disorders in the components of humoral and cellular immunity in the development of intestinal inflammation and amyloidosis in patients with periodical disease. Circulatory disorders, congestive hyperemia, edema of the intestinal mucosa, and spasmodic intestinal dyskinesia that develop during an attack of periodical disease are the initial components in the pathogenesis of inflammatory intestinal lesions seen during periodical disease.

Amyloidosis↗
PubMed1997

[The significance of lactic acid bacteria in treatment and prophylaxis of digestive tract disorders].

Probiotic bacteria are used to treat disturbed intestinal microflora and increased gut permeability which are characteristic to many intestinal disorders. Examples include children with acute rotavirus diarrhoea, subjects with food allergy, subjects with colonic disorders and patients undergoing pelvic radiotherapy and sometimes changes associated with colon cancer development. In all such disease states altered intestinal microflora, impaired gut barrier and different types of intestinal inflammation are present. Successful probiotic bacteria are able to survive gastric conditions and colonise the intestine, at least temporarily, by adhering to the intestinal epithelium. Already existing preparations containing viable lactic bacteria of human origin appear to have value in restoring normal microbial functions and alleviating symptoms in some patients with gastrointestinal infection and other conditions. Current scientifically based research efforts world-wide are now focusing on the development of high quality products containing microorganisms preselected for specific probiotic characteristics.

Child↗
PubMed1987

Involvement of serotonin in intestinal mastocytopoiesis and inflammation during a Trichinella spiralis infection in mice.

The involvement of serotonin in the regulation of intestinal mastocytopoiesis and inflammation has been investigated in mice infected with Trichinella spiralis. Two serotonin antagonists, methysergide and ketanserin, were examined for their ability to interfere with jejunal pathology comprising the influx of mucosal mast cells and other inflammatory cells during an infection with T. spiralis and with worm expulsion. In vitro analysis of the frequency of mast cell precursors in bone marrow, blood, spleen and intestinal tissue suggested that the mucosal mast cell response during a T. spiralis infection is probably due to invasion and local maturation in the gut of mast cell precursors, and may be mediated by T-cell-derived mast cell growth factors. Since both serotonin antagonists inhibited the mucosal mast cell response in T. spiralis-infected mice and diminished the influx of eosinophilic granulocytes, goblet cell hyperplasia, and villous atrophy, it was concluded that during a T. spiralis infection in mice release of serotonin may provide an environment that facilitates the local influx in the gut of inflammatory cells. Since worm expulsion was not affected by the serotonin antagonists, these results suggest that worm expulsion can occur without a mast cell and or eosinophilic granulocyte influx. The role of serotonin release by as yet unidentified serotonin-containing cells in the gut in relation with T cell regulation is discussed.

Animals↗
PubMed1990

Measurements of unsaturated vitamin B12-binding capacity and myeloperoxidase as indices of severity of acute inflammation in serial colonoscopy biopsy specimens from patients with inflammatory bowel disease.

Measurements of tissue content of myeloperoxidase, a constituent of neutrophil azurophil granules and of unsaturated vitamin B12-binding protein from neutrophil-specific granules, have been used to assess intestinal inflammation. This paper reports results of a prospective evaluation of such measurements in serial colonoscopy biopsy specimens from patients with inflammatory bowel disease. Histologic grading of acute inflammation was based on perceived numbers of neutrophil polymorphs in sections from an immediately adjacent biopsy specimen. The mean + 2 SD range for unsaturated vitamin B12-binding protein activity in homogenates of histologically normal specimens was 62 pg mg protein-1. Values increased progressively up to 900 pg mg-1 protein in the most severely inflamed specimens. Unsaturated vitamin B12-binding protein measurements generally distinguished among histologic grades of inflammation, whereas myeloperoxidase activities failed to do this, probably because substantial myeloperoxidase activity was found in uninflamed colonic mucosa, suggesting a non-neutrophil source for this enzyme.

Acute Disease↗
PubMed2005

[Genetic and immunological basis for ulcerative colitis].

Ulcerative colitis is a chronic inflammatory disease of the rectum and colon. Results from many studies in people and animals of intestinal inflammation suggest that ulcerative colitis results from environmental factors triggering a loss of tolerance for normal intestinal flora in genetically susceptible individuals. Although progress has been made in the overall management of the disease, there are few clinical data on biological agents in contrast to Crohn' s disease. Here, we discuss the genetic and immunological basis of ulcerative colitis including the recent findings.

Colitis, Ulcerative↗
PubMed1998

Helicobacter hepaticus triggers colitis in specific-pathogen-free interleukin-10 (IL-10)-deficient mice through an IL-12- and gamma interferon-dependent mechanism.

Mice rendered deficient in interleukin-10 (IL-10) by gene targeting (IL-10(-/-) mice) develop chronic enterocolitis resembling human inflammatory bowel disease (IBD) when maintained in conventional animal facilities. However, they display a minimal and delayed intestinal inflammatory response when reared under specific-pathogen-free (SPF) conditions, suggesting the involvement of a microbial component in pathogenesis. We show here that experimental infection with a single bacterial agent, Helicobacter hepaticus, induces chronic colitis in SPF-reared IL-10(-/-) mice and that the disease is accompanied by a type 1 cytokine response (gamma interferon [IFN-gamma], tumor necrosis factor alpha, and nitric oxide) detected by restimulation of spleen and mesenteric lymph node cells with a soluble H. hepaticus antigen (Ag) preparation. In contrast, wild-type (WT) animals infected with the same bacteria did not develop disease and produced IL-10 as the dominant cytokine in response to Helicobacter Ag. Strong H. hepaticus-reactive antibody responses as measured by Ag-specific total immunoglobulin G (IgG), IgG1, IgG2a, IgG2b, IgG3, and IgA were observed in both WT and IL-10(-/-) mice. In vivo neutralization of IFN-gamma or IL-12 resulted in a significant reduction of intestinal inflammation in H. hepaticus-infected IL-10(-/-) mice, suggesting an important role for these cytokines in the development of colitis in the model. Taken together, these microbial reconstitution experiments formally establish that a defined bacterial agent can serve as the immunological target in the development of large bowel inflammation in IL-10(-/-) mice and argue that in nonimmunocompromised hosts IL-10 stimulated in response to intestinal flora is important in preventing IBD.

Animals↗