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PubMed2006

Agonists of cannabinoid receptor 1 and 2 inhibit experimental colitis induced by oil of mustard and by dextran sulfate sodium.

Oil of mustard (OM) is a potent neuronal activator that is known to elicit visceral hyperalgesia when given intracolonically, but the full extent to which OM is also proinflammatory in the gastrointestinal tract is not known. We have previously shown that male CD-1 mice given a single administration of 0.5% OM develop a severe colitis that is maximum at day 3 and that gradually lessens until essentially absent by day 14. OM-induced neuronal stimulation is reported to be reduced by cannabinoid agonists, and cannabinoid receptor 1 (CB1R)-/- mice have exacerbated experimental colitis. Therefore, we examined the role of cannabinoids in this OM-induced 3-day model of colitis in CD-1 mice and in a 7-day dextran sulfate sodium (DSS) colitis model in BALB/c mice. In OM colitis, the CB1R-selective agonist ACEA and the CB2R-selective agonist JWH-133 reduced (P < 0.05) colon weight gain (means +/- SE; 82 +/- 13% and 47 +/- 15% inhibition, respectively), colon shrinkage (98 +/- 24% and 42 +/- 12%, respectively), colon inflammatory damage score (49 +/- 11% and 40 +/- 12%, respectively), and diarrhea (58 +/- 12% and 43 +/- 11%, respectively). Histological damage was similarly reduced by these treatments. Likewise, CBR agonists attenuated DSS colitis, albeit at higher doses; ACEA at 10 mg/kg, twice daily, inhibited (P < 0.05) macroscopic and microscopic scores (46 +/- 9% and 63 +/- 7%, respectively); whereas 20 mg/kg, twice daily, of JWH-133 was required to diminish (P < 0.05) macroscopic and microscopic scores (29 +/- 7% and 43 +/- 5%, respectively). CB1R and CB2R immunostaining of colon sections revealed that CB1R in enteric neurons was more intense in colitic vs. control mice; however, CB1R was also increased in the endothelial layer in OM colitis only. CB2R immunostaining was more marked in infiltrated immune cells in OM colitis. These findings validate the OM colitis model with respect to the DSS model and provide strong support to the emerging idea that cannabinoid receptor activation mediates protective mechanisms in experimental colitis. The demonstration of CB1R agonist effects in colitis support the neurogenic nature of the OM-induced colitis model and reinforce the importance of neuronal activation in intestinal inflammation.

Animals↗
PubMed1997

Anti-thyroid drugs decrease mucosal damage in a rat model of experimental colitis.

BACKGROUND: Methimazole, an anti-thyroid drug, was recently found to be useful in the treatment of systemic lupus erythematosus and other autoimmune diseases. Moreover, decreased thyroid hormone production is associated with a variety of immunological manifestations, such as reduced activation of CD4+ cells, increased CD8+ cell activity and reduced soluble IL-2 receptors. In the present study we examined the effects of methimazole and propylthiouracil on a rat model of experimental colitis. METHODS: Colitis was induced by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB). Two weeks prior to induction of colitis, rats were treated by either methimaziole (0.04%) or propylthiouracil (0.01%) in drinking water after a week of free access to water. Rats were sacrificed 48 h or 7 days after induction of colitis. The colon was isolated, rinsed with ice-cold water and weighed. Damage was assessed both macroscopically and microscopically and myeloperoxidase (MPO) activity determined. RESULTS: All treated rats were hypothyroid as manifested by a significant elevation of thyroid stimulating hormone (TSH), by comparison with the control groups (mean -1.82 +/- 0.40 versus 0.11 +/- 0.02 mmol/L, respectively). The inflammatory response elicited by TNB resulted in severe mucosal damage 48 h after damage induction, which persisted for 7 days. Pre-treatment with either methimazole 0.04% or propylthiouracil 0.01% significantly decreased mucosal damage macroscopically (lesion area, lesion score and segmental weight) microscopically and also significantly decreased MPO level at both time points (P < 0.01). CONCLUSIONS: Methimazole and propylthiouracil significantly reduce mucosal damage and colonic weight in a rat model of colitis. The mode by which they do so remains to be studied.

Animals↗
PubMed2004

Superoxide dismutase ameliorates TNBS-induced colitis by reducing oxidative stress, adhesion molecule expression, and leukocyte recruitment into the inflamed intestine.

Oxidant stress has been implicated in the pathogenesis of inflammatory bowel disease. Antioxidant enzymes, such as superoxide dismutase (SOD), are candidate drugs for modulating this pathogenic factor. This study was designed to determine the therapeutic value of SOD in an experimental model of colitis and to study the mechanisms underlying its effects on intestinal inflammation. For that purpose, colitic (trinitrobenzene sulfonic acid-induced) and control rats were studied. Groups of colitic animals were treated with different doses of SOD (1, 4, or 13 mg/kg/day) or vehicle, starting after induction of colitis and during 7 days. Clinical and pathological markers of colitis severity and lipid peroxidation in colonic tissue were measured. Leukocyte-endothelial cell interactions in colonic venules and expression of vascular cell adhesion molecule 1 (VCAM-1) were determined. Development of colitis was associated with a significant loss in body weight, an increase in macroscopic and microscopic damage scores, and colonic myeloperoxidase activity. Administration of SOD significantly attenuated these changes in a dose-dependent manner and reduced lipid peroxidation in colonic tissue. The increase in leukocyte rolling and adhesion in colonic venules of colitic rats were significantly reduced by administration of SOD, 13 mg/kg/day. Development of colitis was associated with a marked increase in endothelial VCAM-1 expression, which was significantly reduced by treatment with SOD. In conclusion, treatment with SOD significantly reduces peroxidation reactions in the inflamed colon and affords significant amelioration of colonic inflammatory changes in experimental colitis. This effect is related to a reduction in VCAM-1 expression and leukocyte recruitment into the inflamed intestine.

Animals↗
PubMed2006

The S1P receptor modulator FTY720 prevents the development of experimental colitis in mice.

To evaluate the therapeutic effects of the new synthetic sphingosine-1-phosphate (S1P) receptor modulator, FTY720, we investigated how FTY720 affects the development of dextran sulfate sodium (DSS)-induced colitis and CD4+CD62L+ T cell transfer colitis. BALB/c mice were fed a chow containing 3.5% (wt/wt) DSS to induce colitis. The CD4+CD62L+ T cell transfer colitis was induced by an intraperitoneal injection of CD4+CD62L+ spleen T cells into recipient CB17 SCID mice. The FTY720 was administered by lavage at a dose of 0.3 mg/kg/day. FTY720 was effective in preventing the body weight loss in the DSS-colitis model and the CD4+CD62L+ T cell transfer model. The disease activity index, histological colitis score, and MPO activity were all significantly lower in FTY720-treated mice than in the non-treated mice. Microscopically, mucosal edema, cellular infiltration and epithelial disruption were much more moderate in the FTY720-treated mice than in the non-treated mice. In both colitis models, FTY720 prevented the infiltration of CD4+ T cells into the inflamed colonic lamina propria. In conclusion, the development of DSS-colitis and CD4+CD62L+ T cell transfer colitis were significantly attenuated by FTY720. Since FTY720 is an immunosuppressive product that does not modulate T cell functions, it could be useful in the treatment of IBD patients.

Animals↗
PubMed1989

Causes of death and the histopathologic findings in fatal shigellosis.

Thirty-seven children (median age, 2 years) with shigellosis in Bangladesh were subjected to postmortem examination to determine causes of death and the spectrum of intestinal histopathology. Infecting species were: Shigella dysenteriae 1, 7 cases; S. dysenteriae 2, 2 cases; Shigella flexneri, 23 cases; Shigella boydii, 4 cases; and mixed infection with Shigella boydii and Shigella sonnei, 1 case. Complicating conditions detected before death included malnutrition in 25 cases, pneumonia in 11 cases and septicemia in 8 cases. In all 37 cases the colon showed gross colitis, consisting of mucosal erythema and edema; superficial ulcerations were visible in 15 cases. Microscopically in the colon the lamina propria showed inflammatory cellular infiltration in 27 cases and crypt abscesses were present in 22 cases. In 9 cases each there were colonic glands in the submucosa and branching of colonic crypts, indicating increased regenerative activity of crypt cells. Severe lesions were mucosal denudation and deep ulceration in 15 cases with a pseudomembrane in 7 and pseudopolyposis in 2 of these patients. The most common underlying cause of death was colitis, whereas the most common immediate and associated causes were, respectively, septicemia and pneumonia. These results indicated that fatal childhood shigellosis results from severe colitis, often complicated by septicemia and concomitant malnutrition and pneumonia.

Bangladesh↗
PubMed2005

Therapeutic effect of the immunomodulator glatiramer acetate on trinitrobenzene sulfonic acid-induced experimental colitis.

Inflammatory bowel diseases are characterized by detrimental immune reactivity in the gut and imbalance between proinflammatory and antiinflammatory reactivity. In an attempt to downregulate inflammatory bowel disease, we tested whether the immunomodulator glatiramer acetate (GA; Copaxone, copolymer 1), an approved drug for the treatment of multiple sclerosis, can ameliorate trinitrobenzene sulfonic acid (TNBS)-induced colitis, a murine model that resembles human Crohn's disease. Experimental colitis was induced by rectal instillation of TNBS in 3 mice strains: BALB/c, SJL/J, and (SJL/JXBALB/c)F1, and its severity was evaluated by gross colon injury, histologic damage, body weight, and survival rate. We studied the effect of GA on all these parameters as well as on lymphocyte reactivity manifested by proliferation and secretion of tumor necrosis factor-alpha, and transforming growth factor-beta. GA treatment significantly suppressed the various manifestations of TNBS-induced colitis as demonstrated by substantial reduction in the macroscopic colonic damage, preservation of the microscopic colonic structure, reduced weight loss, and improved long-term survival, in GA treated mice compared with untreated mice. The parenteral route was more effective than the oral route. GA suppressed the proliferation of local mesenteric lymphocytes to syngeneic colon extract and the detrimental tumor necrosis factor-alpha secretion. In addition, it induced a beneficial secretion of transforming growth factor-beta. The ability of GA to effectively modulate the clinical manifestations and the detrimental immune response involved in experimental colitis warrants further studies to determine the clinical efficacy of GA in the treatment of human inflammatory bowel diseases.

Animals↗
PubMed2001

Pathology of inflammatory bowel diseases (IBD): variability with time and treatment.

The diagnosis of chronic idiopathic IBD and the differential diagnosis between Crohn's disease and ulcerative colitis can be made in most cases on cumulative clinical, radiological, endoscopical, biochemical and pathological evidence. Diagnostic difficulties can however, occur in fulminant colitis, in early onset disease and in long-standing disease. The microscopic evaluation of disease activity is based on the presence of active inflammation. Effective medical treatment has however, an influence upon the morphology and the evolution of the lesions and hence can affect the diagnostic features and the microscopic features used for the assessment of disease activity. A literature review was performed on clinical drug trials in IBD and the effect of the drugs upon the microscopic features. Several studies have shown that the diagnostic microscopic features and the features characteristic for disease activity vary with time and treatment. For an adequate analysis of biopsy samples of patients with IBD the pathologist should be aware of the duration of the symptoms and the type of treatment given to the patient.

Journal Article↗
PubMed2004

Prevention of fibrosis in experimental colitis by captopril: the role of tgf-beta1.

BACKGROUND & AIMS: There is a body of evidence to suggest that the local activation of angiotensin II (ANG II) plays a pivotal role in fibrogenic response involving the kidney, heart, lung, pancreas and liver. In such conditions, fibrosis is mediated, at least partially, through ANG II induction of the cytokine transforming growth factor-beta1 (TGF-beta1). Both ANG II and TGF-beta1 also seem to be involved in intestinal fibrosis and stenosis, particularly in Crohn's disease. The aim of the present study was, firstly, to determine the effects of the angiotensin-converting enzyme inhibitor, captopril, on colonic fibrosis in experimental colitis in rats and, secondly, to check the role of TGF-beta1 on these effects. METHODS: Colitis was induced in rats by intracolonic administration of TNBS. Colonic fibrosis was assessed 21 days later by macroscopic and microscopic evaluation. Levels of collagen alpha1 gene expression, hydroxyproline, angiotensin II and TGF-beta1 proteins, and TGF-beta1 mRNA were measured on the colonic tissue. RESULTS: In chronic colitis, captopril significantly reduced the score of macroscopic and histologic lesions, as well as the colonic tissue levels of collagen alpha1, hydroxyproline, ANG II and TGF-beta1 proteins, and TGF-beta1 mRNA. CONCLUSIONS: These data demonstrate for the first time that the prophylactic administration of captopril is effective in preventing colonic fibrosis in TNBS-induced colitis. The antifibrotic action of captopril could be due to the blockade of TGFbeta-1 overexpression, and/or to a direct down-regulation of TGFbeta-1 transcript.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Spontaneous peritonitis from perforation of the colon in collagenous colitis.

A 37-year-old woman presented with an acute abdomen following the onset of watery diarrhea. Spontaneous peritonitis was detected, along with evidence of a focal sigmoid colon perforation. Subsequent postoperative colonoscopic studies revealed collagenous colitis with a focal, deep, nongranulomatous ulcer in the sigmoid colon. Although the literature suggests that collagenous colitis tends to have a relatively 'benign' clinical course characterized by chronic or episodic watery diarrhea. Potentially serious and life- threatening complications may occur in this microscopic form of inflammatory bowel disease.

Adult↗
PubMed1999

Enteric viral infections as a cause of diarrhoea in the acquired immunodeficiency syndrome.

BACKGROUND AND AIMS: The role of non-cytomegalovirus (CMV) enteric viral infection in causing diarrhoea in patients with human immunodeficiency virus (HIV) is poorly understood. We aimed to investigate the prevalence of these infections in acute and chronic diarrhoea. METHODS: Stool specimens from 377 HIV-infected patients presenting with diarrhoea were studied prospectively for evidence of non-CMV enteric viral infection. Patients with diarrhoea underwent investigation for gastrointestinal pathogens, including electron microscopic examination of stool for enteric viruses. We collected data on patients in whom enteric virus was identified and examined the association of enteric virus infection with diarrhoeal symptomatology. RESULTS: Eighty-nine (10.3%) stool specimens from 60 (15.9%) HIV+ individuals were positive for coronavirus (n = 13, 22%), rotavirus (n = 11, 18%), adenovirus (n = 30, 50%) and small round structured viruses (n = 5, 8%) or dual infection (n = 2, 3%). Thirty-four of 52 (65%) patients available for analysis had acute diarrhoea, and 18/52 (35%) had chronic diarrhoea. Twenty-three of 52 (44%) patients had a concurrent gut pathogen. After exclusion of concurrent pathogens enteric viral infections were found to be significantly associated with acute as opposed to chronic diarrhoea (P = 0.004). The presence of adenovirus colitis was significantly more likely to be associated with chronic diarrhoea (15/21 cases) than adenovirus isolated from stool alone (9/23 cases) (P = 0.03). There was a trend towards an association between adenovirus colitis and colonic cytomegalovirus infection (P = 0.06). CONCLUSION: Enteric viral infection is strongly associated with acute diarrhoea in patients with HIV. Light microscopic examination of large bowel biopsies can identify adenovirus colitis which is significantly associated with chronic diarrhoea, and in addition may facilitate gastrointestinal co-infection with CMV.

AIDS-Related Opportunistic Infections↗
PubMed1997

Effect of methylprednisolone on the ulceration, matrix metalloproteinase distribution and eicosanoid production in a model of colitis in the rabbit.

This study has examined the response of a rabbit model of inflammatory bowel disease to methylprednisolone. Colitis was induced in the colon of rabbits with 40 mg trinitrobenzenesulphonic acid in 25% ethanol (TNBS). The effect of methylprednisolone (0.5 mg/kg/day) on the development of colitis was determined at one week, by examining the colon's macroscopic and microscopic appearance, the distribution of matrix metalloproteinases (MMPs) and by measuring eicosanoid production. Although there was no difference in the area of ulcerated colonic tissue in the treated and untreated TNBS animals, the increase in polymorphonuclear leucocytes was significantly reduced in TNBS rabbits given methylprednisolone. The only difference in the distribution of MMPs was a reduction in the number of polymorphonuclear leucocytes containing gelatinase B. The release of immunoreactive PGE2 and LTB4, but not 6-keto PGF1 alpha, was increased in the TNBS animals and was unchanged by methylprednisolone. These results show that methylprednisolone does not modify the injury produced by TNBS in this model despite reducing the infiltration of polymorphonuclear leucocytes. Hence it suggests that these cells do not contribute to the injury observed, are not the source of the eicosanoids and that gelatinase B is not required in the healing process in this model.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Obstructive enterocolitis: a clinico-pathological discussion.

Obstructive colitis is a condition that is not widely appreciated by pathologists. It is defined as an ulcero-inflammatory lesion(s) proximal to a colonic obstruction from which it is separated by a variable length of normal mucosa. Five cases are described which illustrate the clinico-pathological spectrum of the condition. All presented surgically as acute intestinal obstruction, secondary to adenocarcinoma in four cases and a diverticular stricture in one case. Pathologically, the severity of colitis ranged from a single discrete ulcer to an extensive area of fulminant colitis indistinguishable from colitis indeterminate. Furthermore, two cases represented 'obstructive enteritis', a variant of obstructive disease not previously reported. Microscopically, all cases were characterized by distinctive areas of localized ulceration and active inflammation, the features of which were quite unlike those of Crohn's disease or ischaemia, separated by islands of normal mucosa. The role of mural hypoperfusion and secondary localized ischaemia in the pathogenesis of this disorder is discussed. It is suggested that colitis indeterminate represents the final common pathological pathway of the intestine to a wide range of initial insults, be they obstructive or inflammatory.

Adenocarcinoma↗
PubMed1997

Excess glutamine exacerbates trinitrobenzenesulfonic acid-induced colitis in rats.

BACKGROUND: Although the pathogenesis of Crohn's disease remains unclear, an elemental diet has been shown to be clinically effective. Glutamine is an energy source for many cell types including colonocytes. PURPOSE: This study was designed to assess the potential clinical effects on colitis of changing the dietary quantity of glutamine. METHODS: Colitis was induced by intrarectal administration of 30 mg of trinitrobenzenesulfonic acid with 50 percent ethanol vehicle in Sprague-Dawley rats. Rats were randomly allocated into three dietary groups: Group 1, a commercial elemental diet-based diet without glutamine; Group 2, a commercial elemental diet (glutamine: 12 percent of amino acid content); Group 3, elemental diet with 24 percent glutamine. Diets were started one week before colitis induction and continued until sacrifice. Rats were killed at one, three, and five weeks after colitis induction, and colons were excised. Damage evaluation was based on the percentage of rats with ulcer, macroscopic damage score, average ulcer area, and microscopic damage score. RESULTS: Group 2 rats weighed more than Group 1 rats at three weeks because of their higher dietary intake. At one week after colitis induction, all groups had comparable damage. At three weeks, the macroscopic damage score was higher in Group 3 than in Groups 1 and 2. At five weeks, rats in Group 3 had significantly more severe damage than those in Groups 1 and 2 in terms of all four indexes. CONCLUSION: We conclude that excess glutamine has a deleterious effect on ulcers in trinitrobenzenesulfonic acid-induced colitis.

Animals↗
PubMed1987

Acute ischaemic colitis in a female long distance runner.

A 34 year old female long distance runner is reported with bloody diarrhoea. Colonoscopy revealed patchy haemorrhagic mucosal lesions throughout the colon. The most extensive lesions were found in the sigmoid colon. Histologic examination disclosed mucosal haemorrhage, dilated capillaries, patchy fibrosis and superficial erosions. Additional findings in this patient were haemorrhagic gastritis, microscopic haematuria and rhabdomyolysis. The only medication taken by the patient was oral contraceptives. We conclude that ischaemic colitis is one of the possible mechanisms leading to gastrointestinal blood loss in competitive runners.

Acute Disease↗
PubMed2004

Vanilloid receptor 1 antagonists attenuate disease severity in dextran sulphate sodium-induced colitis in mice.

Neurogenic mechanisms have been implicated in the induction of inflammatory bowel disease (IBD). Vanilloid receptor type 1 (TRPV1) has been visualized on nerve terminals of intrinsic and extrinsic afferent neurones innervating the gastrointestinal tract and local administration of a TRPV1 antagonist, capsazepine, reduces the severity of dextran sulphate sodium (DSS)-induced colitis in rats (Gut 2003; 52: 713-9(1)). Our aim was to test whether systemically or orally administered TRPV1 antagonists attenuate experimental colitis induced by 5% DSS in Balb/c mice. Intraperitoneal capsazepine (2.5 mg kg(-1), bid), significantly reduced the overall macroscopic damage severity compared with vehicle-treated animals (80% inhibition, P < 0.05); however, there was no effect on myeloperoxidase (MPO) levels. An experimental TRPV1 antagonist given orally was tested against DSS-induced colitis, and shown to reverse the macroscopic damage score at doses of 0.5 and 5.0 mg kg(-1). Epithelial damage assessed microscopically was significantly reduced. MPO levels were attenuated by approximately 50%, and diarrhoea scores were reduced by as much as 70%. These results suggest that pharmacological modulation of TRPV1 attenuates indices of experimental colitis in mice, and that development of orally active TRPV1 antagonists might have therapeutic potential for the treatment of IBD.

Animals↗
PubMed2004

Effect of cyclosporin A on cell adhesion molecules and leukocyte-endothelial cell interactions in experimental colitis.

BACKGROUND: Cyclosporin A (CsA) is an immunosuppressive agent that is believed to act primarily through effects on T-helper lymphocyte function and proliferation. The aim of this study was to investigate whether modulation of leukocyte recruitment and expression of cell adhesion molecules contribute to the therapeutic efficacy of CsA in a model of experimental colitis. METHODS: The therapeutic effects of CsA were assessed in mice with dextran sulfate sodium-induced colitis. Leukocyte-endothelial cell interactions were determined in colonic venules by intravital microscopy. The expression of cell adhesion molecules intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and mucosal addressin cell adhesion molecule 1 (MAd-CAM-1) was measured by the radiolabeled antibody technique. RESULTS: Treatment with CsA (4 mg/kg/day) significantly improved the clinical course of colitis, decreasing weight loss, diarrhea, rectal bleeding, disease activity index, colon weight, and colonic shortening. Microscopic damage score, myeloperoxidase activity, tumor necrosis factor alpha (TNF-alpha), and interleukin-6 in colonic tissue were significantly diminished by CsA. CsA also significantly reduced ICAM-1 and VCAM-1, but not MAdCAM-1, expression in colitic mice. TNF-alpha-induced ICAM-1 and VCAM-1 expression in primary cultures of human umbilical vein endothelial cells was reduced by co-incubation with CsA. The reduction in adhesion molecule expression was followed by a marked decrease in leukocyte adhesion in colonic venules of colitic mice. CONCLUSIONS: CsA ameliorates experimental colitis in mice. Reduced adhesion molecule expression resulting from diminished pro-inflammatory cytokine production and from a direct effect of CsA in endothelial cells decreases leukocyte recruitment into the inflamed intestine, contributing to this protective effect.

Animals↗
PubMed2005

CD40 antisense oligonucleotide inhibition of trinitrobenzene sulphonic acid induced rat colitis.

BACKGROUND: CD154/CD40 interactions play a pivotal role both in humoral and cellular immune responses. Their involvement in the pathogenesis of chronic inflammatory bowel disease (IBD) has been revealed by increased expression of CD40 and CD154 in the inflamed mucosa of patients and the therapeutic effects of anti-CD154 antibodies in experimental colitis. Because of adverse side effects however, the use of such antibodies in patients with IBD may be limited. AIMS: An alternative approach to blocking CD154/CD40 interactions by employing a CD40 antisense oligonucleotide (ODN) was explored. RESULTS: After sequencing of the rat CD40 gene, five antisense ODNs were designed, of which one (rAS3) effectively downregulated CD40 expression in rat vascular smooth muscle cells as well as the subsequent changes in gene expression in response to CD40 stimulation. The therapeutic potency of rAS3 was evaluated in the 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis model of the rat. Single intracolonic injection of a liposomal formulation of rAS3 either prior to or post colitis induction markedly suppressed the inflammatory reaction in these animals monitored both macroscopically and microscopically over one week, while application of a scrambled control ODN had no such effects. Moreover, reverse transcription-polymerase chain reaction analyses revealed reduced expression of vascular cell adhesion molecule 1, interleukin 12 p40, and monocyte chemoatractive protein 1 in the inflamed mucosa, which in turn may have contributed to the decrease in leucocyte infiltration judged by immunohistochemistry. CONCLUSIONS: These results suggest that CD40 antisense ODNs effectively interfere with CD154/CD40 interactions in vivo and, therefore, may provide a novel approach to the treatment of patients with chronic IBD.

Animals↗
PubMed1977

Fiberoptic endoscopy of the gastrointestinal tract in infants and children. II. Fiberoptic colonoscopy and polypectomy in 15 children.

Fiberoptic colonoscopy was performed on 15 patients between the ages of 1 1/2 years and 16 years. Ten patients were hospitalized and five were outpatients. Of 12 with frank or microscopic blood in stools, fiberoptic colonoscopy revealed single polyps in six patients, ulcerative colitis in two and negative results in four with prior nondiagnostic radiographic studies, colonoscopy revealed ulcerative colitis in one, granulomatous colitis in one and negative findings in one. Polypectomy through the colonoscope was accomplished in all six patients with polyps. Perforation of the sigmoid colon during polypectomy with the snare loop was the single complication encountered. Lower intestinal endoscopy should be selectively considered for diagnosis and therapy of unexplained bleeding or recurrent lower abdominal pain in children in whom proctosigmoidoscopic laboratory and radiographic examinations do not achieve a diagnosis.

Abdomen↗