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PubMed1999

Bacteroides fragilis toxin 2 damages human colonic mucosa in vitro.

BACKGROUND: Strains of Bacteroides fragilis producing a 20 kDa protein toxin (B fragilis toxin (BFT) or fragilysin) are associated with diarrhoea in animals and humans. Although in vitro results indicate that BFT damages intestinal epithelial cells in culture, the effects of BFT on native human colon are not known. AIMS: To examine the electrophysiological and morphological effects of purified BFT-2 on human colonic mucosa in vitro. METHODS: For resistance (R) measurements, colonic mucosa mounted in Ussing chambers was exposed to luminal or serosal BFT-2 (1.25-10 nM) and after four hours morphological damage was measured on haematoxylin and eosin stained sections using morphometry. F actin distribution was assessed using confocal microscopy. RESULTS: Serosal BFT-2 for four hours was four-, two-, seven-, and threefold more potent than luminal BFT-2 in decreasing resistance, increasing epithelial 3H-mannitol permeability, and damaging crypt and surface colonocytes, respectively (p<0.05). Confocal microscopy showed reduced colonocyte F actin staining intensity after exposure to BFT-2. CONCLUSIONS: BFT-2 increases human colonic permeability and damages human colonic epithelial cells in vitro. These effects may be important in the development of diarrhoea and intestinal inflammation caused by B fragilis in vivo.

Actins↗
PubMed2002

Glucagon-like peptide 1 content of intestinal tract in adult rats injected with streptozotocin either during neonatal period or 7 d before sacrifice.

Glucagon-like peptide 1 (GLP-1) content of the intestinal tract was recently found to be lower in diabetesprone BioBreeding (BBdp) rats than in the corresponding control animals (BBc rats), a finding compatible with the idea that an inflammatory intestinal state precedes insulitis in these diabetes-prone animals. This study aimed at measuring GLP-1 content of the intestinal tract both in another animal model of type 1 diabetes and in an animal model of type 2 diabetes. GLP-1 content of the jejunum, ileum, colon, and cecum was measured in male and female adult control rats and animals injected with streptozotocin (STZ) either during the neonatal period or 7 d before sacrifice. GLP-1 content of the intestinal tract was higher in type 1 diabetic rats than in control animals. Such was not the case in the type 2 diabetic rats. The findings recorded in the rats injected with STZ either during the neonatal period or later in life indicate that hyperglycemia and/or insulin deficiency do not cause a decrease in GLP-1 content of the intestinal tract. On the contrary, such a content may increase when the glucose intolerance and hypoinsulinemia are sufficiently pronounced, as was the case in the type 1 diabetic rats. These findings are thus compatible with the view that the decreased GLP-1 content of the intestinal tract in BBdp rats may result from intestinal inflammation.

Animals↗
PubMed2005

Leptin, from fat to inflammation: old questions and new insights.

Leptin is 16 kDa adipokine that links nutritional status with neuroendocrine and immune functions. Initially thought to be a satiety factor that regulates body weight by inhibiting food intake and stimulating energy expenditure, leptin is a pleiotropic hormone whose multiple effects include regulation of endocrine function, reproduction, and immunity. Leptin can be considered as a pro-inflammatory cytokine that belongs to the family of long-chain helical cytokines and has structural similarity with interleukin-6, prolactin, growth hormone, IL-12, IL-15, granulocyte colony-stimulating factor and oncostatin M. Because of its dual nature as a hormone and cytokine, leptin links the neuroendocrine and the immune system. The role of leptin in the modulation of immune response and inflammation has recently become increasingly evident. The increase in leptin production that occurs during infection and inflammation strongly suggests that leptin is a part of the cytokine network which governs the inflammatory-immune response and the host defense mechanisms. Leptin plays an important role in inflammatory processes involving T cells and has been reported to modulate T-helper cells activity in the cellular immune response. Several studies have implicated leptin in the pathogenesis of autoimmune inflammatory conditions, such as experimental autoimmune encephalomyelitis, type 1 diabetes, rheumatoid arthritis, and intestinal inflammation. Very recently, a key role for leptin in osteoarthritis has been demonstrated: leptin indeed exhibits, in concert with other pro-inflammatory cytokines, a detrimental effect on articular cartilage by promoting nitric oxide synthesis in chondrocytes. Here, we review the recent advances regarding leptin biology with a special focus on those actions relevant to the role of leptin in the pathophysiology of inflammatory processes and immune responses.

Animals↗
PubMed2002

A unique subset of self-specific intraintestinal T cells maintains gut integrity.

Lymphocytes residing in the intestinal epithelium are exclusively T cells and account for one of the largest collection of T cells in the organism. However, their function remains obscure. We and others have shown that the development of intestinal intraepithelial T cells is compromised in mutant mice prone to chronic intestinal inflammation. These results led us to directly assess their role in regulating the development of colitis secondary to transfer of primary splenic TCRalphabeta(+)CD4(+)CD45RB(hi) T cells into severe combined immunodeficiency (SCID) mice. Here we demonstrate that prior reconstitution of SCID recipients with intraintestinal TCRalphabeta(+)CD4(-)CD8alpha(+)beta(-) T cells prevents disease, and does so in an interleukin (IL)-10-dependent fashion. In contrast, reconstitution with either TCRgammadelta(+) or TCRalphabeta(+)CD4(-) CD8alpha(+)beta(+) intestinal T cells did not prevent colitis. TCRalphabeta(+)CD4(-)8alpha(+)beta(-) T cells are unique to the intestinal epithelium of both rodents and humans. Previous repertoire analyses of TCRalphabeta(+)CD4(-)CD8alpha(+)beta(-) T cells revealed a high proportion of cells expressing high affinity, self-specific TCR within this subset. We demonstrate that monoclonal, self specific TCRalphabeta(+)CD4(-)CD8alpha(+)beta(-) cells derived from TCR transgenic mice also prevent the onset of colitis. Thus, intestinal TCRalphabeta(+)CD4(-)CD8alpha(+)beta(-) T cells, selected based on their self-reactivity, maintain gut integrity in a IL-10-dependent fashion.

Animals↗
PubMed2004

Differential effect of immune cells on non-pathogenic Gram-negative bacteria-induced nuclear factor-kappaB activation and pro-inflammatory gene expression in intestinal epithelial cells.

We have previously shown that non-pathogenic Gram negative bacteria induce RelA phosphorylation, nuclear factor (NF)-kappaB transcriptional activity and pro-inflammatory gene expression in intestinal epithelial cells (IEC) in vivo and in vitro. In this study, we investigated the molecular mechanism of immune-epithelial cell cross-talk on Gram-negative enteric bacteria-induced NF-kappaB signalling and pro-inflammatory gene expression in IEC using HT-29/MTX as well as CaCO-2 transwell cultures Interestingly, while differentiated HT-29/MTX cells are unresponsive to non-pathogenic Gram negative bacterial stimulation, interleukin-8 (IL-8) mRNA accumulation is strongly induced in Escherichia coli- but not Bacteroides vulgatus-stimulated IEC cocultured with peripheral blood (PBMC) and lamina propria mononuclear cells (LPMC). The presence of PBMC triggered both E. coli- and B. vulgatus-induced mRNA expression of the Toll-like receptor-4 accessory protein MD-2 as well as endogenous IkappaBalpha phosphorylation, demonstrating similar capabilities of these bacteria to induce proximal NF-kappaB signalling. However, B. vulgatus failed to trigger IkappaBalpha degradation and NF-kappaB transcriptional activity in the presence of PBMC. Interestingly, B. vulgatus- and E. coli-derived lipopolysaccharide-induced similar IL-8 mRNA expression in epithelial cells after basolateral stimulation of HT-29/PBMC cocultures. Although luminal enteric bacteria have adjuvant and antigenic properties in chronic intestinal inflammation, PBMC from patients with active ulcerative colitis and Crohn's disease differentially trigger epithelial cell activation in response to E. coli and E. coli-derived LPS. In conclusion, this study provides evidence for a differential regulation of non-pathogenic Gram-negative bacteria-induced NF-kappaB signalling and IL-8 gene expression in IEC cocultured with immune cells and suggests the presence of mechanisms that assure hyporesponsiveness of the intestinal epithelium to certain commensally enteric bacteria.

Animals↗
PubMed1993

Guinea pig ileitis is attenuated by the leumedin N-(fluorenyl-9- methoxycarbonyl)-leucine (NPC 15199).

Anti-inflammatory properties have been ascribed to a series of N-(fluorenyl-9-methoxycarbonyl) amino acids called leumedins that inhibit the activity of granulocytes and T-lymphocytes. We evaluated one of these leumedins, N-(fluorenyl-9-methoxycarbonyl) leucine (NPC 15199), in a model of ileitis in guinea pigs. Ileitis was induced by intraluminal trinitrobenzenesulfonic acid (TNBS 30 mg/kg in 50% ethanol) in anesthetized guinea pigs. NPC 15199 was administered daily (10 or 100 mg/kg, s.c.). After 7 days, the guinea pigs were anesthetized, and saline was administered intraluminally into an ileal loop created at the site of TNBS administration and was withdrawn after 30 min. The changes in lavage protein, nitrite levels, myeloperoxidase (MPO) activity and mast cell numbers were used as indices of inflammation and injury. NPC 15199 (10 or 100 mg/kg) attenuated or abolished TNBS-induced elevations in lavage protein and nitrite content. Only the high dose of NPC 15199 (100 mg/kg) attenuated ileal MPO activity and mast cell hyperplasia. Histological disturbances induced by TNBS administration included crypt hypertrophy, mucosal and submucosal fibrosis and smooth-muscle hyperplasia. These disturbances were reversed by high-dose NPC 15199 (100 mg/kg) but were minimally affected by low-dose NPC 15199 (10 mg/kg). We conclude that NPC 15199 prevents mucosal injury and dysfunction in this model of intestinal inflammation. Inhibition of granulocyte infiltration does not appear to be essential for the beneficial effects of NPC 15199 and suggests that the alternative actions of NPC 15199 may be pertinent to this model.

Animals↗
PubMed1997

Number, fixation properties, dye-binding and protease expression of duodenal mast cells: comparisons between healthy subjects and patients with gastritis or Crohn's disease.

There is an accumulation of evidence to suggest that mast cells may play a key role in gastrointestinal inflammation. We have investigated the numbers and heterogeneity in staining properties of mast cells in biopsies of the duodenum of normal subjects (n = 10), and of normal duodenum from patients with Crohn's disease of the ileum and/or colon (n = 7) or with Helicobacter-associated gastritis of the antrum/corpus (n = 6). In normal donors, two subsets of mast cells, one located in the duodenal mucosa and the other in the submucosa, were clearly distinguished by their morphology and dye-binding properties. Whereas submucosal mast cells stained metachromatically with Toluidine Blue after neutral formalin fixation and emitted a yellow fluorescence after staining with Berberine sulphate, those in the mucosa were invisible using these stains. In patients with gastritis or Crohn's disease, there were marked changes in the numbers of mucosal mast cells compared with control subjects even though the duodenal biopsies were from apparently uninvolved tissue. Gastritis was associated with increased mucosal mast cell numbers (controls: 187 +/- 23 cells mm-2; gastritis: 413 +/- 139 cells mm-2; p = 0.0004), but mean mucosal mast cell counts in the uninvolved duodenum of Crohn's patients were actually decreased (34 +/- 30 cells mm-2, p = 0.0147). The clear differentiation between mucosal and submucosal mast cells on the basis of metachromasia with Toluidine Blue was not seen in biopsies from the patients with gastritis or Crohn's disease. Previous studies which have suggested that there are no distinct mucosal and submucosal mast cell subsets in the human intestine may, therefore, have been affected by the use of tissue from diseased subjects. Heterogeneity in the expression of mast cell tryptase and chymase was seen by immunohistochemistry using specific antibodies, but the relative numbers of mast cell subsets were critically dependent on the methods used. Using a sensitive staining procedure, the majority of mucosal mast cells stained positively for chymase as well as for tryptase, an observation confirmed by immunoelectron microscopy and immunoabsorption studies. Our findings suggest that early stages in intestinal inflammation may be reflected in changes in mast cell numbers and in their staining properties, and call for a reappraisal of mast cell heterogeneity in the human intestinal tract.

Adult↗
PubMed2005

Acute toxicity of nano- and micro-scale zinc powder in healthy adult mice.

The purpose of this study is to evaluate the acute toxicity of oral exposure to nanoscale zinc powder in mice. The healthy adult male and female mice were gastro-intestinally administered at a dose of 5 g/kg body weight with two size particles, nanoscale zinc (N-Zn) and microscale zinc (M-Zn) powder, while one group mice treated with sodium carboxy methyl cellulose was used as the control. The symptoms and mortality after zinc powder treatment were recorded. The effects of particles on the blood-element, the serum biochemical level and the blood coagulation were studied after 2 weeks of administration. The organs were collected for histopathological examination. The N-Zn treated mice showed more severe symptoms of lethargy, vomiting and diarrhea in the beginning days than the M-Zn mice. Deaths of two mice occurred in the N-Zn group after the first week of treatment. The mortalities were confirmed by intestinal obstruction of the nanoscale zinc aggregation. The biochemical liver function tests of serum showed significantly elevated ALT, AST, ALP, and LDH in the M-Zn mice and ALT, ALP, and LDH in the N-Zn mice compared with the controls (P<0.05), which indicated that the liver damage was probably induced by both micro- and nano-scale zinc powders. The clinical changes were observed in the two treated group mice as well. The levels of the above enzymes were generally higher in the M-Zn mice than in the N-Zn mice, which implied that M-Zn powder could induce more severe liver damage than N-Zn. The biochemical renal function tests of serum BUN and CR in the M-Zn mice markedly increased either compared with the N-Zn mice or with the controls (P<0.05), but no significant difference was found between the N-Zn and the control mice. However, severe renal lesions were found by the renal histopathological examination in the N-Zn exposed mice. Therefore, we concluded that severe renal damage could occur in the N-Zn treated mice, though no significant change of blood biochemical levels occurred. Blood-element test showed that in the N-Zn mice, PLT and RDW-CV significantly increased, and HGB and HCT significantly decreased compared to the controls, which indicated that N-Zn powder could cause severe anemia. Besides the pathological lesions in the liver, renal, and heart tissue, only slight stomach and intestinal inflammation was found in all the zinc treated mice, without significant pathological changes in other organs.

Animals↗
PubMed2000

Inducible nitric oxide synthase: a little bit of good in all of us.

The established dogma regarding the different isoforms of nitric oxide has been that constitutively expressed nitric oxide synthase is an extremely important homeostatic regulator of numerous important physiological processes whereas the inducible form of nitric oxide synthase underlies injury associated with intestinal inflammation. In this brief overview, I review some of the literature that clearly supports this contention, particularly the dramatically beneficial effects of oral L-NAME administration to animals with colitis induced by trinitrobenzene sulphonic acid (TNBS). However, I also highlight some of the gastrointestinal data that does not fit this simple tidy paradigm, particularly with respect to the inducible form of nitric oxide synthase (iNOS). For example, iNOS induced healing of skin and the intestinal mucosa, killing of certain bacteria, regulation of T cell proliferation and differentiation (Th1 v Th2), and control of leucocyte recruitment may mask or counter the toxic metabolites that are produced by iNOS. Perhaps it is not surprising that one does not always obtain benefit from inhibiting all iNOS either by gene deletion or by systemic NOS inhibition. I raise some potential flaws in our approaches to studying iNOS. For example, to date no attempts have been made to selectively inhibit iNOS in single cell types. Global inhibition of all iNOS assumes that the large variety of cell types that can produce iNOS have identical functions. Finally, I attempt to highlight areas that require additional investigation and issues that have not been explored.

Animals↗
PubMed1999

Role for IL-4 in macromolecular transport across human intestinal epithelium.

Increased epithelial permeability is associated with intestinal inflammation, but there is little information on factors that regulate barrier function in the absence of or before inflammation. We examined if interleukin (IL)-4, or serum from atopic individuals, could alter the barrier function of human colonic epithelial (T84) monolayers to antigenic-sized macromolecules. IL-4 and atopic serum significantly decreased T84 monolayer resistance and increased transepithelial horseradish peroxidase (HRP) transport. Bidirectional transport studies demonstrated that IL-4 selectively enhanced apical-to-basal movement of HRP. HRP transport induced by IL-4 was inhibited by cold (4 degrees C) and the tyrosine kinase inhibitor genistein, but not the protein kinase C inhibitor staurosporine. Electron microscopic analysis demonstrated that both transcellular and paracellular pathways were affected. Anti-IL-4 antibodies abolished the increase in HRP transport in response to both IL-4 and serum. We speculate that enhanced production of IL-4 in allergic conditions may be a predisposing factor to inflammation by allowing uptake of luminal antigens that gain access to the mucosal immune system.

Adult↗
PubMed2004

Impairment of intestinal intraepithelial lymphocytes in Id2 deficient mice.

BACKGROUND: Id2, an inhibitor of basic helix-loop-helix transcription factors, regulates cell differentiation. Id2-/- mice exhibit a variety of phenotypes in the immune system. AIMS: In this study we investigated whether Id2 plays a role in intestinal intraepithelial lymphocytes (IELs), which constitute the main defence against pathogens in the intestinal tract. METHODS: Flow cytometry and bone marrow transplantation were used to analyse and characterise subsets of IELs of Id2-/- mice. Gene expression was analysed by real-time polymerase chain reaction. Intestinal barrier function was evaluated by treating mice with 5-fluorouracil (5-FU). RESULTS: Among the four members of the Id gene family, Id2 was selectively expressed in all T cell subsets in the small intestinal IELs. Id2-/- mice showed alteration in the proportions of T cell subsets and a substantial reduction in the number of IELs, especially those of the CD4+ and CD8 alpha beta+ T cell subsets, indicating a more pronounced effect on thymus derived IELs. Expression of alphaE integrin was reduced in CD4+ and CD8 alpha beta+ T cell subsets in IELs of Id2-/- mice. IELs isolated from C57BL/6 mice reconstituted with Id2-/- bone marrow cells showed a similar phenotype to that of Id2-/- mice, indicating that the defects are intrinsic to bone marrow derived cells. Expression of genes encoding intestinal epithelial cell derived cytokines was reduced in Id2-/- mice. The 5-FU treatment revealed impaired intestinal barrier function of Id2-/- mice. CONCLUSIONS: The Id2 gene is essential for constituting the intestinal mucosal barrier, particularly with respect to IELs. Id2 null mutant mice may provide a good experimental model for studying the ontogeny of IELs and intestinal inflammation and infection.

Animals↗
PubMed2003

Rationale for probiotic and antibiotic treatment strategies in inflammatory bowel diseases.

Inflammatory bowel diseases (IBD), commonly referred to as Crohn's disease and ulcerative colitis are chronic aggressive disorders which share many similarities concerning pathomechanism and clinical course, but have very distinct features. Both entities are mainly located in areas with high bacterial concentrations, such as the terminal ileum and cecum in Crohn's disease and the rectum in ulcerative colitis. In recent years, overwhelming evidence accumulated, supporting the hypothesis that IBD are characterized by a genetically determined, overly aggressive immune response towards ubiquitous luminal antigens, especially commensal bacteria and their products. Trials in both human IBD and experimental colitis have demonstrated that broad-spectrum antibiotics may influence the course of ulcerative colitis and Crohn's disease and antibiotics with narrow activity against the anaerobic fraction of the flora can prevent relapse in Crohn's disease after surgically induced remission. Since relevant antibiotic strategies can be associated with some side effects, the ongoing research recently focused on alternative methods to modify the intestinal flora in patients with IBD. Clinical observations including few controlled trials, basic research, and animal studies have suggested a potential role for probiotic bacteria within the treatment regimens for IBD. However, the mode of action of these organisms is still largely unclear and in vitro studies are inconclusive. This review summarizes recent in vitro and in vivo data regarding the role of the intestinal microflora in the pathogenesis of chronic intestinal inflammation and possible therapeutic mechanisms of probiotic bacteria relevant to IBD. Furthermore, we will review clinical trials examining the efficacy of antibiotic and probiotic treatment strategies in IBD.

Anti-Bacterial Agents↗
PubMed2005

The intestinal flora in inflammatory bowel disease: normal or abnormal?

PURPOSE OF REVIEW: The human gut is the natural habitat for a large and dynamic bacterial community. There is a substantial body of evidence implicating the resident flora in the pathogenesis of chronic intestinal inflammation. This review discusses the possible role of a microbial imbalance in the pathophysiology of inflammatory bowel disease. RECENT FINDINGS: Recently developed molecular biologic tools suggest that a sizeable part of the microbial populations of the human gut remains to be defined. Conversely, the relevance of gut bacteria in the host's physiology is well documented. The specialised lymphoid follicles of the gut mucosa are the major sites for induction of effector and regulatory mechanisms of the intestinal immune system, and it is now becoming clear that resident and in-transit microorganisms play an essential role in the homeostasis of local and systemic immunity. An infectious origin of inflammatory bowel disease is not supported by our current knowledge. Several studies, however, have disclosed substantial differences in the intestinal flora between patients with inflammatory bowel disease and healthy subjects, in regard to both composition and mucosal colonisation. Aggressive species are abundant on the inflammatory bowel disease mucosal surface whereas protective genera are underrepresented, but the biologic relevance of these changes needs further investigation. SUMMARY: A balanced microbial environment would likely help in both prevention and control of inflammatory bowel disease. Research is needed to identify microorganisms able to mediate immunoregulation in the gut mucosa.

Bacteria, Aerobic↗
PubMed2004

Attenuation of acute experimental colitis by preventing NPY Y1 receptor signaling.

Neuropeptide Y (NPY), a 36-amino acid peptide, is widely expressed in the central and peripheral nervous system. NPY is involved in the regulation of several physiological processes, including energy balance, food intake, and nociception. Recently, we showed that activation of the NPY Y1 receptor is required for cutaneous neurogenic inflammation. Because neurogenic inflammation could participate in colitis, the aim of this study was to investigate the role of the NPY Y1 receptor in acute colitis using mice genetically deficient of NPY Y1 receptor. In addition, the Y1 receptor antagonist H409/22, was also investigated. Animals received 5% dextran sulfate sodium (DSS) in drinking water for 7 days. One group of animals also received the Y1 receptor antagonist, administered intraperitoneally twice daily. Disease activity was assessed daily for 7 days in all groups. DSS induced colitis in all animals resulting in weight loss, diarrhea, epithelial damage, crypt shortening, and inflammatory infiltration. However, clinical manifestation of the disease was markedly attenuated in Y1 null mutant mice as well as in mice receiving the Y1 antagonist. Histological analysis showed that tissue damage and ulceration were less severe in Y1-deficient animals. Consistent with the clinical and histological data, capsaicin-induced plasma extravasation was significantly reduced in the gut of Y1 null mutant animals compared with treated wild-type animals. These data indicate that NPY and Y1 receptor are involved in intestinal inflammation and suggest that inhibition of NPY Y1 receptor signaling may provide a novel therapeutic approach in the treatment of colonic inflammation.

Acute Disease↗
PubMed2004

Immune regulation in the intestine: a balancing act between effector and regulatory T cell responses.

The immune system in the intestine must respond rapidly to invading pathogens without mounting sustained effector cell responses to the indigenous commensal bacteria. Results from this laboratory using the T cell transfer model of colitis suggest that specialized populations of regulatory T cells control the immune response in the intestine. Regulatory T (Tr) cell activity is enriched within the naturally arising CD4(+) CD25(+) Tr subset that has been shown to prevent a number of inflammatory diseases. CD4(+) CD25(+) Tr cells control intestinal inflammation induced by both innate and adaptive immune responses via IL-10- and TGF-beta-dependent mechanisms. Recent results have shown that CD4(+) CD25(+) Tr cells can cure established colitis, suggesting their utility for the treatment of inflammatory bowel disease.

Animals↗
PubMed2005

Helminths and the modulation of mucosal inflammation.

PURPOSE OF REVIEW: Inflammatory bowel disease is an emerging illness associated with socioeconomic development. The current epidemic of immune-mediated diseases may result from our loss of exposure to parasitic worms (helminths). This review summarizes some of the recent findings showing that helminths induce regulatory circuits that could prevent and treat inflammatory bowel disease. RECENT FINDINGS: Inflammatory bowel disease appears to result from a dysregulated immune response. Although genes influence the risk of inflammatory bowel disease, it seems that critical changes in our environment have permitted its expression. One such change is the eradication of helminths. Helminths can impede interleukin-12, interferon gamma, and tumor necrosis factor alpha release and promote interleukin-10, transforming growth factor beta, and regulatory T-cell production. Helminths can prevent and reverse intestinal inflammation in animal models of inflammatory bowel disease. In clinical studies of patients with inflammatory bowel disease, exposure to the helminth Trichuris suis reduces disease activity. SUMMARY: If harboring helminths protects against immune-mediated disease, then these animals must be viewed in a new light. Are there "good" helminths in addition to bad? Instead of being detestable objects marked for eradication, helminths should be viewed as useful animals that may produce important compounds helpful for therapy of human disease.

Animals↗
PubMed2002

Nitric oxide supplementation ameliorates dextran sulfate sodium-induced colitis in mice.

Nitric oxide (NO) synthesis is up-regulated in inflammatory bowel disease. However, its role in the pathophysiology of this condition is controversial. The aims of this study were to assess whether nitric oxide administration ameliorates experimental colitis and to determine the possible mechanisms underlying its effects on intestinal inflammation. For this purpose, the NO donor diethylamine NONOate (DETA/NO; 0.01, 0.1, 1, 5, or 10 mg/kg/day), or the DETA moiety, was administered daily to mice with dextran sulfate sodium-induced colitis. Daily body weight and colonic pathologic alterations at Day 10 were determined. Leukocyte endothelial cell interactions in colonic venules were assessed with intravital microscopy, and expression of endothelial cell adhesion molecules was determined using radiolabeled antibodies. IL-12 and IFN-gamma production were measured in intestinal tissue. Colitis induced a significant loss of body weight, reduction of colon length, and increase in colon weight and myeloperoxidase activity. Administration of 1 mg/kg/day DETA/NO significantly attenuated these pathologic changes. The marked increase in leukocyte rolling and adhesion in colonic venules of colitic mice were significantly reduced by administration of 1 mg/kg/day DETA/NO. Development of colitis was associated with a marked increase in endothelial expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and P-selectin. Supplementation with NO significantly attenuated the up-regulation of endothelial intercellular adhesion molecule-1 and P-selectin, but not vascular cell adhesion molecule-1, in colonic tissue. NO abrogated the increase in IL-12 and IFN-gamma mRNA expression in the colon of colitic mice. The DETA moiety alone did not have any effect on any of the parameters studied. In conclusion, exogenous NO supplementation significantly ameliorates dextran sulfate sodium-induced colitis. This effect is related to a reduction in leukocyte recruitment and proinflammatory cytokine production.

Animals↗
PubMed2006

Enterolithiasis in a cat.

An 8-year-old female Persian cat was brought in for evaluation of chronic vomiting. The presence of opaque enteric foreign bodies and intestinal obstruction along with azotaemia, hyperphosphataemia, moderate anaemia and peritoneal fluid were revealed following appropriate diagnostic work-up. Exploratory laparotomy confirmed jejunoileal dilation, ileocaecal stenosis, and numerous foreign objects in the jejunoileum. These foreign objects and ileocaecal stenosis were surgically removed, and intestinal resection and anastomosis was performed. The patient recovered favourably. Analysis revealed that the foreign objects were composed of calcium phosphate and calcium carbonate. Intestinal inflammation and stenosis secondary to enterolithiasis may have developed following ingestion of cat litter or a previous unrelated surgical intervention. We were unable to delineate the inciting pathogenesis in this particular case.

Animals↗