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PubMed2002

Role of IL-10 in hepatocyte tight junction alteration in mouse model of experimental colitis.

BACKGROUND: A variety of hepatobiliary abnormalities have been described in patients with chronic inflammatory bowel diseases (IBDs). The purpose of this study was to investigate the role of endogenous IL-10 in alteration of hepatocyte TJ paracellular barrier and in the rapid transcytotic vesicular pathway modification associated with intestinal inflammation. MATERIALS AND METHODS: To address this question, we used an experimental model of colitis, induced by dinitrobenzene sulfonic acid (DNBS). When compared to DNBS-treated IL-10 wild-type (IL-10WT) mice, DNBS-treated IL-10 knock-out mice (IL-10KO) mice experienced a higher rate of the extent and severity of the histological signs of colon injury. RESULTS: Colon and liver levels of the pro-inflammatory cytokines tumour necrosis factor, interleukin-1 beta and interleukin-6 were also greatly enhanced in IL-10KO mice in comparison to wild-type mice. Liver histology from IL-10KO and IL-10WT did not show any parenchymal and portal tract inflammation at 4 days after DNBS administration. Serum total bilirubin and Alanine aminotransferase, were significantly increased in DNBS-IL-10KO mice vs. DNBS-IL-10KO mice. Therefore, we found an increase of tight junctional permeability to lanthanum nitrate (molecular weight, 433) in the livers from DNBS-treated IL-10WT mice; lanthanum accumulated throughout the junctional area up to the most apical region bordering the lumen. Absence of a functional IL-10 gene in IL-10KO mice resulted in a significant augmentation of apical diffusion of lanthanum after DNBS-induced colitis. Immunofluorescent labelling of frozen liver sections from DNBS-IL10KO mice, immunolocalization for and claudin-1 and ZO-1 resulted in a significant alteration in the localization of the immunosignals for claudin-1 and ZO-1 after DNBS administration in comparison with DNBS-IL10WT. CONCLUSION: In conclusion, we suggest that the absence of IL-10 may represent an important pathophysiological mechanism of hepatobiliary injuries and cholestasis observed in patients with IBD.

Alanine Transaminase↗
PubMedDate not supplied

[Chronic intestinal inflammatory diseases].

In the last years the research on the etiopathogenesis of the inflammatory bowel disease (IBD) is focused around immunological aspects. Many authors consider that the intestinal inflammation is due to an inappropriate immunological response to normally present antigens in the gut. Two aspects must to be considered between IBD: Crohn's disease and ulcerative colitis. IBD's diagnosis is based on the symptomatology, (cramps, liquid feces with mucus and blood, anorexia and weight loss), hemato-clinical tests (ESR, PCR, blood platelet, mucoprotein, sideremia) and radiological tests (tenuis Rx, abdominal echography, fibro endoscophy and scintigraphy). Principal aim of the therapy is the clinical remission. Following the remission starts a maintenance protocol. Parenteral nutrition is used in paediatric and adolescent age. Diets have been used to provide a convenient nutritious contribution with growth improvement and partial remission of activity index of the disease. Pharmacology therapy represents a valid instrument to obtain the remission. Colectomy is performed on unsuccessful medical therapy. Early studies on IBD's pathogenesis bring to the use of biological therapies that show beneficial effects on the disease.

Humans↗
PubMed2003

Interleukin-8, tumor necrosis factor-alpha, and lactoferrin in immunocompetent hosts with experimental and Brazilian children with acquired cryptosporidiosis.

To examine the importance of intestinal inflammation in the diagnosis and pathogenesis of human cryptosporidiosis, stools of healthy adult volunteers before and after experimental infection were tested for fecal lactoferrin, interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha). Stool samples of Brazilian children with well-defined Cryptosporidium infection, with or without diarrhea, were also tested for IL-8 and TNF-alpha. Only one of the 14 volunteers challenged with Cryptosporidium had increased fecal lactoferrin. However, of 17 stool specimens from children with only Cryptosporidium infection from a previous study, 12 had mild to moderately elevated lactoferrin despite negative work-up for inflammatory enteritides. One of 10 adult volunteers who developed diarrhea with experimental cryptosporidiosis and three of 11 children with cryptosporidiosis and diarrhea had detectable fecal IL-8. The level of TNF-alpha was increased only in one of 14 volunteers and in none of the children. Although considered relatively non-inflammatory. cryptosporidiosis is often associated with mild inflammation, especially in children in an endemic area.

Adult↗
PubMed2003

Role of iNOS in hepatocyte tight junction alteration in mouse model of experimental colitis.

A variety of hepatobiliary abnormalities occur in inflammatory bowel diseases (IBDs). The role of tight junction (TJ) in hepatobiliary complications have been well described. The purpose of this study was to investigate the role of inducible nitric oxide (NOS) in alteration of hepatocyte TJ paracellular barrier and in the rapid transcytotic vesicular pathway modification associated with intestinal inflammation. To address this question, we used an experimental model of colitis, induced by dinitrobenzene sulfonic acid (DNBS). When compared to DNBS-treated iNOS wild-type (WT) mice, DNBS-treated iNOS knock out mice (iNOSKO) mice experienced a significant less rate of the extent and severity of the histological signs of colon injury. Colon levels of the pro-inflammatory cytokines tumour necrosis factor, interleukin-1beta and interleukin-6 were also significantly reduced in iNOS-KO mice in comparison to wild-type mice. Liver histology from iNOSKO and wild-type mice iNOSWT did not show any parenchymal and portal tract inflammation at 4 days after DNBS administration. Serum total bilirubin and alanine aminotransferase, were significantly reduced in DNBS-iNOSKO mice vs DNBS-iNOSKO mice. Therefore, we found an increase of tight junctional permeability to lanthanum nitrate (molecular weight, 433) in the livers from DNBS-treated IL-10WT mice, lanthanum accumulated throughout the junctional area up to the most apical region bordering the lumen. Absence of a functional iNOS gene in iNOSKO mice resulted in a significant reduction of apical diffusion of lanthanum after DNBS-induced colitis. Immunofluorescent labeling of frozen liver sections from DNBS-iNOSWT mice showed a significant alteration of the immunolocalization for claudin-1 and zonula occludens (ZO)-1. In contrast, a significant reduced alteration in the localization of the immunosignals for claudin-1 and ZO-1 was observed in the liver from iNOSKO mice after DNBS administration. In conclusion, we suggest that the iNOS may represent an important pathophysiological mechanism of hepatobiliary injuries and cholestasis observed in patients with IBD.

Animals↗
PubMed2003

Experimental models of inflammatory bowel disease.

The etiology and pathogenesis of inflammatory bowel disease (IBD) remains unsolved, but improved experimental models of enterocolitis have led to progress. Intestinal inflammation and experimental IBD can be induced by chemical or dietary factors or by microbial products. Many animal models of IBD can be used to evaluate new anti-inflammatory drugs. These models, however, usually demonstrate acute, self-limiting colitis. The spontaneous colitis models developed in the cotton-top tamarin monkey and the C3H/HeJBir mouse mimic more features of human IBD. Inflammation is chronic and is under genetic control. The differential genetic susceptibility of inbred rat strains to chronic inflammation have been exploited. Lewis rats injected with bacterial products, peptidoglycan polysaccharide or indomethicin develop chronic relapsing enterocolitis, whereas closely related Buffalo or Fisher rat strains develop only transient inflammation. These models are also useful to test the specific inhibition of inflammatory mediators and target molecules. Over-expression (transgenic) or deletion (knockout) of specific genes have led to the development of rodent models of spontaneous colitis. Inflammation arises from a number of mutations of immunomodulatory molecules, supporting the concept of genetic heterogeneity for IBD. The results obtained from experimental models have generated new hypotheses, expanded human studies, and suggested novel forms of therapy for IBD patients.

Animals↗
PubMedDate not supplied

Simultaneous assays for Clostridium difficile and faecal lactoferrin in ulcerative colitis.

Infectious agents may be one of the important factors in initiating or perpetuating ulcerative colitis. Increasing evidence has accumulated regarding the role of Clostridium difficile (C. difficile) infection in the exacerbation of ulcerative colitis. The present work was undertaken to study the implications of C. difficile toxin (CDT) and faecal lactoferrin (FL) positivity in patients with idiopathic ulcerative colitis (IUC) in a north Indian hospital. Ninety-four faecal samples from patients of IUC were processed for CDT and FL simultaneously. Clinical details of patients, including antibiotic intake in the past 6 weeks, were recorded. Eighty-one of the 94 patients (86.2%) had diarrhoea and 48 (51.1%) had received antibiotics. There was a statistically significant (p < 0.001) increase in the prevalence of diarrhoea among individuals receiving antibiotics. Twelve of the 94 samples (12.8%) were CDT positive while 16 were FL positive. No statistical significance (p > 0.05) was seen while comparing the positivity of CDT and FL in relation to the receipt of antibiotics. A statistically significant (p < 0.001) positive correlation was present between CDT and FL assays. FL positivity in IUC may depend on the intestinal inflammation precipitated by C. difficile infection.

Adolescent↗
PubMed1992

[Angiotensin-converting-enzyme (ACE) in Crohn's disease].

Serum concentration of angiotensin-converting enzyme (ACE) were measured in 34 patients with Crohn's disease. ACE was decreased in Crohn's disease compared with healthy controls. Significant negative regression between ACE and CDAI was observed. It suggested intestinal ACE may play a regulatory role in intestinal inflammation of Crohn's disease. Among the patients, ACE did not show the significant change by use of prednisolone nor by location of disease. The mechanism of ACE decrease in Crohn's disease was not known, but this phenomena may be one of the reason of persistent inflammation of Crohn's disease.

Adult↗
PubMed2003

N-3 fatty acid-rich diet prevents early response of interleukin-6 elevation in trinitrobenzene sulfonic acid-induced enteritis.

Dietary fat is an important factor involved in the pathogenesis of inflammatory bowel disease (IBD). It remains unclear how n-3 and n-6 fatty acids modulate intestinal inflammation. In this study, we investigated the effects of n-3 and n-6 fatty acid-rich diets on trinitrobenzene sulfonic acid (TNBS)-induced enteritis. The rats were fed an n-3 or n-6 rich-diet for 12 days, and then starved for the following 2 days. An intraileal injection of TNBS was administered, and TNBS-enteritis subsequently developed. Macroscopic and histological examination was performed after 24 h. Serum cytokine levels were determined by ELISA. The n-6 fatty acid-rich diet markedly enhanced mucosal damage as compared to the n-3 fatty acid-rich diet. The damage score was significantly higher in the n-6 fatty acid-rich diet group (P<0.05). Histological changes in the mucosa were more severe in the n-6 fatty acid-rich diet group than in the n-3 fatty acid-rich group. Serum IL-6 levels were significantly higher in the n-6 fatty acid-rich diet group than in the n-3 fatty acid-rich group (P<0.05). On the other hand, there were no differences in serum TNF-alpha levels. The n-3 fatty acid-rich diet effectively reduced early mucosal inflammation in TNBS enteritis. The effects of the n-3 fatty acids were associated with blockage of mucosal IL-6 secretion. Our data suggest that n-3 fatty acid-rich diet may be applicable for enteral nutrition in the treatment of IBD patients.

Animal Feed↗
PubMed2003

[Osteoporosis and inflammatory bowel disease: prevalence and risk factors in Tunisian patients].

OBJECTIVES: The study was aimed to evaluate osteoporosis prevalence in a group of Tunisian patients with inflammatory bowel disease (IBD), to determine its risk factors, and to describe its mechanisms. SUBJECTS AND METHODS: We included 67 IBD patients, 43 patients with Crohn's disease (CD) and 24 with ulcerative colitis (UC). Bone mineral density was measured at the lumbar spine and left femoral neck by dual-energy X-ray absorptiometry. We used T score to express bone loss (osteopenia: -2.5 SD 2 years and active disease tended to be associated with lumbar osteoporosis; the ORs were respectively 4.87 [0.92-25.80] (P=0.06), 4.21 [0.87-20.57] (P=0.06), and 2.33 [0.78-6.67] (P=0.13). No association was found with cumulated dose of steroids even when considering only CD. Patients with osteoporosis showed significant increased CrossLaps and interleukin-6 levels that indicate both high bone resorption and inflammatory activity. CONCLUSIONS: Osteoporosis is frequent in IBD patients, especially in CD patients. Female gender, malnutrition (body mass index <20 kg/m2), disease course (> 2 years) and active disease would be risk factors of bone mineral loss in IBD. Osteoporosis is associated with enhanced bone resorption, that seems be linked to excessive intestinal inflammation.

Adolescent↗
PubMed2003

[Calprotectin: a fecal marker for diagnosis and follow-up in patients with chronic inflammatory bowel disease].

Chronic inflammatory bowel disease (IBD) is characterised clinically by periods of well being interspersed by exacerbations of disease activity. Differentiation between IBD and less severe disorders such as irritable bowel syndrome requires invasive and expensive diagnostic procedures. Diagnostic differentiation between active disease, symptoms due to residual constriction of the fibrotic lumen and functional symptoms is a well-known problem. There are not yet any laboratory parameters with sufficient discrimination in terms of sensitivity and specificity. Colonoscopy and histopathological examination remain the gold standards: in Crohn's disease this may be complex due to the variable localisation of the inflammatory process. Abdominal scintigraphic procedures, although informative, are complex and expensive. The recent assessment of faecal calprotectin, a calcium- and zinc-binding anti-inflammatory protein found in neutrophilic granulocytes and monocytes, offers an attractive alternative as an index of intestinal inflammation. We measured this stable marker in random stool samples from 187 patients including healthy volunteers, patients with endoscopically classified active IBD or IBD in remission, and patients with other gastrointestinal disorders. Disease activity was monitored by clinical symptoms, blood tests and endoscopy. Our results confirm previous literature findings that faecal calprotectin is a promising and useful non-invasive tool in the screening of patients presenting with abdominal pain and diarrhoea. Moreover, calprotectin seems helpful in differentiating between active and non-active IBD and possibly also in the monitoring of disease activity.

Biomarkers↗
PubMed2004

[Association between the cytotoxic T lymphocyte antigen-4 gene microsatellite polymorphism and inflammatory bowel diseases in the Chinese].

OBJECTIVE: Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation as a result of an exaggerated T-cell response. Cytotoxic T lymphocyte antigen-4 (CTLA-4) expressed mainly on activated T cells, inhibits T cell activation by combining B(7) through competing CD(28) and maintains immune system homeostasis. Polymorphisms in the CTLA-4 gene are known to be associated with several autoimmune diseases, but no studies related to IBD. The aim of the study is to investigate an association between CTLA-4 gene microsatellite polymorphisms and IBD. METHODS: Unrelated 68 Chinese Han patients with IBD (54 ulcerative colitis and 14 Crohn's disease) and 140 healthy controls were studied. The (AT)n repeat sequence in the 3' untranslated region of exon 4 were amplified by allele-specific PCR. The amplified products were electrophorosised by 12% polyacrylamid gel and followed by silver staining. RESULTS: Eighteen alleles of CTLA-4 microsatellite were found in Chinese patients and healthy individuals. Long allele, 122bp was apparently increased in patients with ulcerative colitis compared with healthy controls (7.4% vs 0.3%, P = 0.0002/Pc = Sig, OR = 22.32, 95% CI: 2.76 - 180.80). CONCLUSION: CTLA-4 gene microsatellite polymorphism was strongly associated with ulcerative colitis in Chinese Han patients in Hubei province.

Adult↗
PubMed2005

Inflammatory bowel disease.

BACKGROUND: Inflammatory bowel disease (IBD) is increasing in frequency in Australia. General practitioners play an important role in early diagnosis and in a multidisciplinary approach to managing such patients. Keeping abreast of evolving concepts, particularly in treatment, is challenging. OBJECTIVE: This article aims to address key issues in diagnosis and management to better equip general practitioners for their role in multidisciplinary management of patients with IBD. DISCUSSION: Making the diagnosis can be difficult, but is facilitated by appropriate clinical suspicion and sensible judgment as to who undergoes diagnostic tests such as colonoscopy. Treatment of ulcerative colitis has changed little in recent years, except for our improved ability to deliver mesalazine to the large bowel via the recent availability of several oral and rectal preparations. Prevention of relapse using these is an important strategy in the majority of patients. Treatment of Crohn disease is changing due to more realistic concepts of the natural history of the disease and the development of new, powerful anti-inflammatory therapies. Attention to issues other than intestinal inflammation such as nutrition, education and counselling, remain important in achieving optimal management.

Adrenal Cortex Hormones↗
PubMed2002

Pharmacogenomics in gastrointestinal disorders.

Genomic techniques offer new approaches to the investigation of the aetiology and pathophysiology of intestinal disorders. An important field that is relevant to treatment is the pharmacogenetic investigation of gene variations that may predict response to certain drugs in order to target these drugs more precisely. For the surgeon the perioperative situation will be here of great interest. To date only about 8000 of the estimated 30,000-50,000 human genes have been characterised, so the use of techniques for global analysis of gene expression may allow the identification of new pathways or molecules. In can be anticipated that genomic methods will profoundly influence the treatment of gastrointestinal disorders and will lead to new insights into both aetiology and pathophysiology of chronic intestinal inflammation.

Gastrointestinal Diseases↗
PubMed2005

[Erythema nodosum].

The authors describe a case of 41-year-old patient with erythema nodosum as a manifestation of colitis ulcerosa. They stress the importance of complex look at this skin disease, which can be caused by many factors. Non-specific intestinal inflammation can be a cause of the erythema nodosum in 1-2%.

Adult↗
PubMed2006

Protective effect of geranylgeranylacetone on trinitrobenzene sulfonic acid-induced colitis in mice.

Geranylgeranylacetone (GGA) has recently been reported to have a protective effect against ischemic, injurious and apoptotic stress in several tissues. The aim of this study was to determine the effect of GGA on colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. Colitis was induced by intrarectal instillation of TNBS in 50% ethanol in BALB/c mice. Survival, change in body weight and change in wet colon weight were assessed. Histological score in the colon was evaluated 5 days after TNBS treatment. The level of myeloperoxidase (MPO) activity in the colon was also determined. Immunohistochemistry for CD4 in the colon was performed. In addition, the level of heat shock protein (HSP) 70 in the colon was determined by Western blot analysis. Mice were orally treated with GGA (300 mg/kg) 2 h before and every other day after starting TNBS administration. Treatment with GGA markedly improved the survival rate, and reduced the loss of body weight and loss of wet colon weight in mice with TNBS-induced colitis. GGA also suppressed the increase in MPO activity and the number of CD4-positive cells infiltrating the colons of mice with TNBS-induced colitis. Furthermore, treatment with GGA remarkably up-regulated the expression of HSP70 in the colons of mice with TNBS-induced colitis. Our results provide further evidence that GGA has therapeutic potential for intestinal inflammation.

Animals↗
PubMed2006

Pro-inflammatory signaling by Jun-N-terminal kinase in inflammatory bowel disease.

Since Jun-N-terminal kinase participates in intracellular signaling cascades resulting in inflammatory responses, inhibiting this pathway may represent a new treatment for inflammatory bowel disease including ulcerative colitis and Crohn's disease. However, the functional significance of the activation of this kinase in inflammatory bowel disease remains unclear. We investigated whether Jun-N-terminal kinase activation is increased in inflammatory bowel disease and analyzed the effects of SP600125, which decreases inflammatory cytokine synthesis by inhibiting the phosphorylation of this kinase. Phosphorylation of the kinase was examined in affected human colon using an enzyme-linked immunosorbent assay and immunohistochemistry. The effect of SP600125 on cytokine production was examined in cultures of patients' leukocytes and colonic tissue. Finally, rats received injection of SP600125 (30 mg/kg, s.c.) or vehicle twice daily 2 h before the induction of colitis with dextran sulfate sodium. SP600125 effects were determined observationally and histologically. Colonic tissue contained increased phosphorylated kinase in patients with inflammatory bowel disease with expression localized to the nucleus of epithelial and lamina propria mononuclear cells in lesions. Culturing mononuclear cells or colonic tissue with SP600125 down-regulated inflammatory cytokine production. Prophylactic treatment with SP600125 significantly reduced clinical and pathological scores in dextran sulfate sodium-treated rats. This first demonstration of the pathogenetic role of Jun-N-terminal kinase in the development of intestinal inflammation suggests that inhibiting its phosphorylation could benefit patients with inflammatory bowel disease.

Animals↗
PubMed2006

[Probiotics].

While the precise pathophysiology of IBS remains to be elucidated, dysmotility and altered visceral perception/sensation are currently the most popular hypotheses. More recently, roles for enteric infection and intestinal inflammation have been proposed. Probiotics, defined as live or attenuated bacteria or bacterial products that confer a significant health benefit to the host, have the potential to provide a clinical tool to explore these interactions. We reviewed the effects of probiotics on IBS symptoms.

Humans↗