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PubMed1996

Differential expression of cysteine-rich intestinal protein in liver and intestine in CCl4-induced inflammation.

Cysteine-rich intestinal protein (CRIP) is a double zinc finger (LIM domain) protein that is developmentally regulated but has an unknown function. CRIP is highly expressed in the intestine, but expression is low in liver. To determine if CRIP expression is regulated under altered physiological status, we used CCl4-induced injury as a model to produce hepatic injury and systemic effects associated with inflammation. Since CRIP is a zinc finger protein and zinc decreases the hepatic response to CCl4, the effect of supplemental dietary zinc (300 mg/kg diet) was also examined. Our results show that this supplemental level of dietary zinc did not affect the index of hepatic injury (plasma alanine aminotransferase), indicating zinc did not have a protective effect. Liver CRIP mRNA increased with CCl4 and CRIP protein was shown by immunohistochemistry to be localized in hepatocytes near the vascular supply. In the intestine, CCl4 caused a transient decrease in CRIP mRNA, but supplemental dietary zinc treatment prevented this decrease. These current results show that CRIP expression changes in response to cellular damage due to acute hepatic injury and are consistent with a functional role for CRIP in proliferation, differentiation, or turnover.

Animals↗
PubMed2001

Dietary vitamin E supplementation protects the rat large intestine from experimental inflammation.

Vitamin E, the most potent antioxidant in the lipid phase, was tested for antiinflammatory activity in trinitrobenzenesulfonic acid-induced rat colitis. Rats were fed a nonpurified diet (saline and control groups) or a vitamin E supplemented diet (treated group, 300 mg/kg nonpurified diet). Vitamin E supplementation, which resulted in increased colonic vitamin E levels, reduced colonic weight and damage score, prevented lipid peroxidation and diarrhea, reduced interleukin-1 beta levels and preserved glutathione reductase activity and total glutathione levels. However, it did not modify myeloperoxidase levels, which are indicative of neutrophil infiltration in the inflamed colon. Vitamin E protects the rat colon from oxidative stress associated with inflammation.

Animals↗
PubMed1985

Intestinal giardiasis associated with ocular inflammation.

A relationship between intestinal giardiasis and ocular inflammatory conditions may result in significant vision loss. The parasitic infestation may not produce gastrointestinal symptoms and since early eradication of the parasite may prevent permanent visual loss, it is important that gastroenterologists as well as ophthalmologists be aware of this association.

Adult↗
PubMed2002

Probiotics: a role in the treatment of intestinal infection and inflammation?

Probiotic therapy is based on the concept of normal healthy microflora. The development of novel means of characterising the gut microflora, in particular those based on the different levels of conservation in the ribosomal RNA sequences of different genera, have opened up new angles on the role of the gut microflora in health and disease. Components of the human intestinal microflora or organisms entering the intestine may have harmful or beneficial effects on human health. Abundant evidence implies that specific strains selected from the healthy gut microflora exhibit powerful antipathogenic and anti-inflammatory capabilities, and are consequently involved with enhanced colonisation resistance in the intestine. Realisation of this has led to the introduction of novel modes of therapeutic and prophylactic intervention based on the consumption of mono and mixed cultures of beneficial live microorganisms as probiotics.

Acute Disease↗
PubMed2004

Role of probiotics in the modulation of intestinal infections and inflammation.

PURPOSE OF REVIEW: Using microorganisms to influence positively the course of an illness caused by injurious microorganisms is an approach with mounting clinical evidence showing efficacy. Whereas antibiotics will remain an important therapeutic option, there are limitations and problems to their increasing and chronic usage, and probiotics offer a strategy to reduce antibiotic usage. Increasingly, it has become clear that the mechanisms whereby probiotics can impact in intestinal diseases involve a large repertoire of responses. This review summarizes recent findings on how probiotics may effect benefit through interactions with host eukaryotic cells. RECENT FINDINGS: Limiting the access of microbes associated with the development of disease to host mucosal surfaces and altering the responses of host to microbial insults are potential mechanisms whereby probiotics can influence the pathogenesis of disease. Evidence is accumulating that live, viable probiotic organisms diminish accessibility to intestinal epithelial cell; however, the mucosal exclusion is not through direct blockage of shared epithelial receptors between probiotic microbes and pathogenic organisms. Modulation of mucosal defenses such as innate protective mechanisms, enhanced epithelial cell survival, and immune responses have all been shown to have potential in aiding in these actions. Intestinal epithelial cell adherence influences response and, as such, appears to be necessary but may not be wholly sufficient, because soluble bacterial factors have been reported to effect modulation of immune and nonimmune responses of eukaryotic cells. SUMMARY: There is a considerable repertoire of responses potentially responsible for the effects of probiotics, and these responses appear to involve a complex interplay between the microbes of the intestinal tract and the cells of the host. Continued work can be expected to further the understanding of the mechanisms involved, and more work is needed to determine the relative clinical importance of each of the phenomena. These studies are expected to help direct the most efficacious use of probiotics for inflammatory conditions arising from the intestinal tract.

Journal Article↗
PubMed2002

Role of probiotics in the treatment of intestinal infections and inflammation.

Despite the relative success of analogous approaches in soil, aquatic, and animal environments, the enhancement of human health through probiotic consumption has not been generally endorsed in modern medicine. Laboratory-based studies are elucidating the mechanisms that mediate the properties attributed to beneficial lactic acid bacteria and Saccharomyces species in vivo. This research is now providing fundamental evidence to support observations of adhesion of probiotic species to intestinal tissue, antimicrobial activities, and immunomodulation. Probiotics appear to have a promising future in the treatment of certain disorders. Rigorously performed, controlled, double-blinded trials will overcome doubts relating to efficacy in vivo and open avenues along which probiotic-based therapies will rapidly progress. As a result of our emerging understanding of microbial activities and gene expression in situ, novel strategies will combine complementary probiotic functionalities in the form of microbial consortia or genetically enhanced organisms. As scientific knowledge and biotechnologic proficiency advance at an accelerating pace, the requirement for informed legislation and for mechanisms of effectively delivering these therapies to the sites of their intended function may limit the applications of probiotics.

Journal Article↗
PubMed2005

CD4+ T cell mediated intestinal immunity: chronic inflammation versus immune regulation.

BACKGROUND: Several studies have suggested that chronic inflammatory bowel disease may be a consequence of antigen specific recognition by appropriate T cells which expand and induce immunopathology. AIMS: We wished to investigate whether autoreactive CD4+ T cells can initiate the disease on recognition of enterocyte specific antigens directly and if induction of mucosal tolerance occurs. METHODS: Transgenic mice (VILLIN-HA) were generated that showed specific expression of haemagglutinin from influenza virus A exclusively in enterocytes of the intestinal epithelium. To investigate the impact of enterocyte specific haemagglutinin expression in an autoimmune environment, we mated VILLIN-HA mice with T cell receptor (TCR)-HA mice expressing an alpha/beta-TCR, which recognises an MHC class II restricted epitope of haemagglutinin, and analysed the HA specific T cells for induction of autoimmunity or tolerance. RESULTS: In VILLIN-HAxTCR-HA mice, incomplete central deletion of HA specific lymphocytes occurred. Peripheral HA specific lymphocytes showed an activated phenotype and increased infiltration into the intestinal mucosa, but not into other organs of double transgenic mice. Enterocyte specific lamina propria lymphocytes showed a dose dependent proliferative response on antigen stimulation whereas the proliferative capacity of intraepithelial lymphocytes was reduced. Mucosal lymphocytes from VILLIN-HAxTCR-HA mice secreted lower amounts of interferon gamma and interleukin (IL)-2 but higher levels of tumour necrosis factor alpha, monocyte chemoattractant protein 1, and IL-6. Mucosal immune reactions were accompanied by broad changes in the gene expression profile with expression of proinflammatory genes, but strikingly also a remarkable set of genes discussed in the context of peripheral induction of regulatory T cells, including IL-10, Nrp-1, and Foxp3. CONCLUSIONS: Enterocyte specific antigen expression is sufficient to trigger a specific CD4+ T cell response leading to mucosal infiltration. In our model, progression to overt clinical disease was counteracted most likely by induction of regulatory T cells.

Animals↗
PubMed2004

A novel potent inhibitor of inducible nitric oxide inhibitor, ONO-1714, reduces intestinal ischemia-reperfusion injury in rats.

The overproduction of nitric oxide (NO) by inducible nitric oxide synthase (iNOS) may contribute to the pathophysiology of intestinal injury induced by ischemia-reperfusion. The aim of the present study was to examine the effect of selective iNOS inhibition by a cyclic amidine analogue, ONO-1714, on reperfusion-induced small intestinal injury and inflammation in rats. Intestinal damage was induced in male Sprague-Dawley rats by clamping both the superior mesenteric artery and the celiac trunk for 30 min, followed by reperfusion. The luminal nitrite concentration in the small intestine was measured by Griess reaction and the iNOS mRNA expression by RT-PCR. The severity of the intestinal mucosal injury and inflammation were evaluated by several biochemical markers and by the histological findings. The rats which were killed after ischemia-reperfusion had increased luminal concentrations of nitrite and iNOS mRNA expression, in addition to severe intestinal inflammation characterized by significant increases in myeloperoxidase activity, a marker of neutrophil infiltration, and by the mucosal content of CINC-1 cytokine, a neutrophil chemotactic cytokine. Administration with ONO-1714 significantly inhibited the luminal NO production. Reperfusion after 30-min ischemia resulted in an increase in luminal protein and hemoglobin concentrations, with levels reaching a maximum after 60 min of reperfusion. In contrast, pre-treatment with ONO-1714 2h before the ischemia inhibited the increases in luminal protein and hemoglobin concentration in a dose-dependent manner (0.001-0.1mg/kg). The contents of the thiobarbituric acid-reactive substances (a marker of oxidative lipid peroxidation) were significantly increased by ischemia-reperfusion, and this increase was reduced by ONO-1714. After reperfusion, the increase in tissue-associated myeloperoxidase activity, an index of neutrophil infiltration, was significantly inhibited by pre-treatment with ONO-1714. ONO-1714 also inhibited increases in intestinal CINC-1 protein and mRNA expression, as determined by ELISA and RT-PCR, respectively. In conclusion, the improvement of reperfusion-induced intestinal injury by ONO-1714 suggested that an excess of NO, produced by iNOS, may have contributed to the initiation/amplification of intestinal inflammatory injury by various mechanisms, including nitrosative and oxidative damage as well as the enhancement of inflammatory cytokine release.

Amidines↗
PubMed1997

Review article: Homing of mucosal immune cells--a possible connection between intestinal and articular inflammation.

An adaptive immune system has developed to protect mucosa, mainly by performing immune exclusion with secretory antibodies (SIgA and SIgM) but also by downregulating pro-inflammatory antibody responses and delayed type hypersensitivity against harmless soluble proteins and the indigenous bacterial flora. In general, mucosal immunopathology appears to represent abrogation of such mucosal tolerance mechanisms. An important consequence is disturbance of the 'gatekeeper' function normally performed by the microvasculature through complementary sets of tightly regulated adhesion molecules on mucosal endothelium and circulating leukocytes. The B cells responsible for local polymeric immunoglobulin (Ig) production (mainly dimeric IgA) are stimulated initially in organized lymphoepithelial structures, particularly the Peyer's patches in the distal small intestine, from which they migrate as memory cells to secretory tissues all over the body. Mucous membranes are thus furnished with primed B cells in an integrated way, ensuring a variety of secretory antibody specificities at every exocrine site. There is currently great interest in exploiting this integrated or 'common' mucosal immune system for topical vaccination against pathogenic infectious agents and also to induce therapeutic peripheral tolerance to ameliorate T-cell-mediated autoimmune diseases. Moreover, homing of immune cells from the gut to the inflamed synovium may represent a modifiable link between intestinal immunity and chronic arthropathies.

Arthritis↗
PubMed2006

New insights into the biological and clinical significance of fecal calprotectin in inflammatory bowel disease.

Nowadays, calprotectin, a cytoplasmatic protein, released by activated neutrophilic polymorphonuclear cells (PMN) and/or monocytes-macrophages (MØ), is considered a good indicator of inflammation in several diseases. Accordingly, fecal calprotectin represents a good predictor of clinical relapse in ulcerative colitis (UC) patients, whereas conflicting results have been reported in Crohn's disease (CD) patients. In our study, in 76 IBD patients (29 CD and 47 UC) fecal calprotectin has been evaluated by a commercial ELISA kit. Results demonstrate that levels of this protein in the stool are significantly more elevated in active CD and UC patients than in normal volunteers. In quiescent CD and UC a trend to higher levels of calprotectin than in the normal counterpart is, however, evident. These data suggest that a low-grade inflammation of the intestinal wall is always present in CD and UC patients, which may predict a clinical relapse risk. In the same group of patients calprotectin levels also were analyzed according to sex and age. A trend to higher values of calprotectin was present in male patients with active or quiescent CD than in their female counterparts. Only in UC patients in remission a trend to calprotectin increase was more marked in the male group than in the female counterpart. When CD and UC patients were divided up according to age, calprotectin positivity peaked between 30-39 years in active CD patients, while in quiescent CD maximum positivity was between 40 and 49 years. However, in both active and quiescent UC patients, calprotectin positivity increased with age. The more precocious detectability of fecal calprotectin in CD patients, as a marker of intestinal mucosa inflammation, may be related to the different histopathology of the two diseases (CD versus UC). However, reduced PMN and/or MØ trafficking from peripheral blood to intestinal mucosa with age by effects of chronic treatment should not be ignored in CD patients.

Adolescent↗
PubMedDate not supplied

Inflammatory bowel disease and the eye.

Inflammatory bowel disease includes Crohn's disease and ulcerative colitis, and is characterized by chronic inflammation of the intestines. The advances in understanding of the inflammatory process have resulted in improved treatment of inflammatory bowel disease. The systemic complications of inflammatory bowel disease involve many organs, eyes included. The ophthalmic complications are usually of inflammatory origin. Some of these complications, like scleritis, may reflect overall disease activity. Treatment of intestinal inflammation-either medical or surgical-usually helps resolution of ophthalmic complications. This review describes recent developments in the diagnosis and management of the inflammatory bowel disease and its ophthalmic complications.

Colitis, Ulcerative↗