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PubMed1998

Fulminant jejuno-ileitis following ablation of enteric glia in adult transgenic mice.

To investigate the roles of astroglial cells, we targeted their ablation genetically. Transgenic mice were generated expressing herpes simplex virus thymidine kinase from the mouse glial fibrillary acidic protein (GFAP) promoter. In adult transgenic mice, 2 weeks of subcutaneous treatment with the antiviral agent ganciclovir preferentially ablated transgene-expressing, GFAP-positive glia from the jejunum and ileum, causing a fulminating and fatal jejuno-ileitis. This pathology was independent of bacterial overgrowth and was characterized by increased myeloperoxidase activity, moderate degeneration of myenteric neurons, and intraluminal hemorrhage. These findings demonstrate that enteric glia play an essential role in maintaining the integrity of the bowel and suggest that their loss or dysfunction may contribute to the cellular mechanisms of inflammatory bowel disease.

Animals↗
PubMed2001

[Laparoscopic diagnosis of stenosing eosinophilic jejuno-ileitis].

INTRODUCTION: Eosinophilic gastroenteritis of unknown origin could be isolated or integrated in idiopathic hypereosinophilic syndrome. Clinical expression is variable since the lesion may affect any area of the gastrointestinal tract and any layer of the wall. EXEGESIS: A 25-year-old male patient had digestive symptoms such as peritoneal, obstructive and diarrheal signs, associated with blood eosinophilia, giving evidence for eosinophilic jejuno-ileitis. Computer tomography revealed an extensive obstruction of the jejuno-ileum and thickening of the intestinal wall. The diagnosis was obtained using laparoscopy and controlled wedge biopsy, which showed a predominantly external infiltration of the intestinal wall by eosinophils. The disease evolution was favorable with corticosteroid therapy. CONCLUSION: Worrying and persistent digestive symptomatology, associated with blood eosinophilia, particularly when intestinal wall infiltration is revealed by computer tomography, should lead one to perform a laparoscopy to guide a surgical biopsy of the intestinal wall.

Adrenal Cortex Hormones↗
PubMed2004

Ursodeoxycholic acid ameliorates experimental ileitis counteracting intestinal barrier dysfunction and oxidative stress.

The aim of this study was to evaluate the effect of ursodeoxycholic acid (UDCA) on intestinal permeability (IP) and reactive oxygen species (ROS) generation in indomethacin-induced enteropathy, a well-known experimental model of Crohn's disease. Seventy-eight male Wistar rats were randomly assigned to receive indomethacin, indomethacin + UDCA, or vehicles. Indomethacin induced a significant increase in the fraction of urinary excretion of 51Cr-EDTA following oral administration (7.9 +/- 1.3 vs 2.3 +/- 0.2%; P < 0.05) and lucigenin-amplified chemiluminescence in intestinal fragments ex vivo (10.1 +/- 1.9 vs 2.6 +/- 0.4 cpm x 10(3)/mg; P < 0.05) compared to controls. UDCA significantly reversed these effects (P < 0.05), without being incorporated in biliary bile acid composition (HPLC analysis). These findings support a local protective effect of UDCA in experimental ileitis by the modulation of intestinal barrier dysfunction and oxidative stress. In short, they provide insights into mechanisms of action of UDCA in intestinal inflammation and a new perspective on the treatment of Crohn's disease.

Animals↗
PubMed1998

Resection for CMV ileitis in a patient supported by a left-ventricular assist device.

We describe a patient requiring a HeartMate 1000 IP left-ventricular assist device (LVAD) due to cardiogenic shock. After prolonged gastrointestinal bleeding without identifying the source of bleeding technetium scintigraphy pointed to the right lower abdomen. The patient underwent a laparotomy and inflamed ileum was resected. Pathologic examination revealed cytomegalovirus ileitis. This was treated with ganciclovir and acyclovir. The patient is now (14 months later) awaiting heart transplantation since she could not be weaned from LVAD. The diagnostic and management problems are discussed as well as the relevance for future transplantation.

Adult↗
PubMed1993

[Life-threatening arterial bleeding in hemorrhagic-necrotizing salmonella ileitis].

A 23-year-old man in otherwise good health had diarrhoea for two days during a holiday on Maldives. Two months later he suddenly collapsed and had to be admitted to hospital. Haemoglobin concentration was found to be 76 g/l, with a haematocrit of 0.22, WBC count of 17,800/microliters and platelets of 22%. Massive passage of bright red blood in the stools (none previously) could not be explained by abdominal sonography, oesophagogastroduodenoscopy, coloscopy, technetium scintigraphy or angiography of the superior mesenteric artery. Exploratory laparotomy revealed severe inflammatory changes in the terminal ileum with enlargement of the regional lymph-nodes and spurting bleeding from a branch of the ileocolic artery. Histological examination showed focal necrotizing, ulcerative and haemorrhagic ileitis. After ileocaecal resection and end-to-end anastomosis to the ascending colon the patient quickly recovered. Salmonella Livingstone was isolated from the stool and the infection was treated with ciprofloxacin, 200 mg twice daily intravenously for 5 days. Subsequent stool samples were negative but follow-up continues.

Adult↗
PubMed2006

Role of TL1A and its receptor DR3 in two models of chronic murine ileitis.

TL1A is a TNF-like cytokine that binds to the death-domain receptor (DR)3 and provides costimulatory signals to activated lymphocytes. Through this interaction, TL1A induces secretion of IFN-gamma and may, therefore, participate in the development of T helper-1-type effector responses. In this study, we investigated whether interactions between TL1A and DR3 are involved in the pathogenesis of chronic murine ileitis. We demonstrate that alternative splicing of DR3 mRNA takes place during the activation of lymphocytes, which results in up-regulation of the complete/transmembrane (tm) form of DR3. Using two immunogenetically distinct animal models of Crohn's disease, we demonstrate that induction of intestinal inflammation is associated with significant up-regulation of TL1A and tm DR3 in the inflamed mucosa. In addition, within isolated lamina propria mononuclear cells from mice with inflammation, TL1A is primarily expressed on CD11c(high) dendritic cells. We also report that TL1A acts preferentially on memory CD4(+)/CD45RB(lo) murine lymphocytes by significantly inducing their proliferation, whereas it does not affect the proliferation of the naïve CD4(+)/CD45RB(hi) T helper cell subpopulation. Finally, we demonstrate that TL1A synergizes with both the cytokine-dependent IL-12/IL-18 pathway and with low-dose stimulation of the T cell receptor to significantly induce the secretion of IFN-gamma via an IL-18-independent pathway. Our results raise the possibility that interaction(s) between TL1A expressed on antigen-presenting cells and tm DR3 on lymphocytes may be of particular importance for the pathogenesis of chronic inflammatory conditions that depend on IFN-gamma secretion, including inflammatory bowel disease. Blockade of the TL1A/DR3 pathway may, therefore, offer therapeutic opportunities in Crohn's disease.

Alternative Splicing↗
PubMed2003

TNF-alpha neutralization ameliorates the severity of murine Crohn's-like ileitis by abrogation of intestinal epithelial cell apoptosis.

Tumor necrosis factor alpha (TNF-alpha) is an important mediator of programmed cell death, and TNF-alpha blockade significantly improves disease severity in several inflammatory conditions, including Crohn's disease (CD), one of the idiopathic inflammatory bowel diseases. However, the precise mechanism(s) of action of anti-TNF-alpha therapy in CD remains poorly understood. SAMP1/YitFc mice develop a spontaneous ileitis with similarities to human CD in regard to histological features as well as response to conventional treatments. In this report, we tested the novel hypothesis that the beneficial effects of anti-TNF-alpha therapy in CD are mediated by a mechanism that involves down-regulation of intestinal epithelial cell (IEC) apoptosis. Similar to the efficacy of monoclonal anti-TNF-alpha antibodies in human CD, a single injection of a chimeric anti-murine TNF-alpha antibody into SAMP1/YitFc mice resulted in a marked suppression of intestinal inflammation and epithelial cell damage compared with mice injected with an isotype control antibody. These effects were associated with a significant reduction in apoptosis of freshly isolated IEC as assessed by propidium iodide staining and DNA laddering. In contrast, an increase in lamina propria mononuclear cell apoptosis was observed in anti-TNF-alpha-treated mice compared with control. These results were confirmed in vivo by using the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling-assay. In addition, neutralization of TNF-alpha reduced membrane bound FAS/CD95 expression in IEC from SAMP1/YitFc mice compared with control antibody. These data demonstrate a novel mechanism of action of anti-TNF-alpha therapy that involves homeostatic regulation of mucosal cell apoptosis, which results in the net decrease of chronic inflammation typically found in CD.

Animals↗
PubMed1986

Gold-induced ileitis.

We describe a patient with rheumatoid arthritis who developed severe ileitis after being treated with gold salts; the patient responded to elimination of the gold therapy and to BAL.

Arthritis, Rheumatoid↗
PubMed2006

Asymptomatic ileitis: past, present, and future.

We critically review the limited data on an emerging clinical entity, asymptomatic ileitis. We discuss some of the current theorized etiologies of this phenomenon, including subclinical Crohn's disease, nonsteroidal anti-inflammatory drugs, and spondylarthropathies. Finally, we discuss future areas of investigation that may better help identify and evaluate this increasingly common finding.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Persistent ileitis after ileal salvage from a failed Kock pouch.

A case of persistent ileitis following the refashioning of a Kock ileal pouch into a Brooke ileostomy for severe pouchitis is reported. Preserving the terminal ileum by a salvage procedure may not be a safe alternative to pouch excision with the formation of a new end ileostomy in the surgical management of pouchitis refractory to medical treatment.

Adult↗
PubMed2005

Cytologic diagnosis of Lawsonia intracellularis proliferative ileitis in a Japanese snow macaque (Macaca fuscata).

Diffuse ileal thickening and ileocecocolic lymphadenomegaly were observed during exploratory laparotomy in a 2-year-old male Japanese snow macaque (Macaca fuscata) that had flu-like signs and diarrhea. Cytologic examination of ileal biopsy imprints revealed many mature, mildly karyolytic neutrophils and fewer well-differentiated lymphocytes, eosinophils, macrophages, and plasma cells in a background containing amorphous, necrotic material. Tightly cohesive sheets of moderately pleomorphic epithelial cells also were seen. The cytologic diagnosis was chronic, active, mixed inflammation with atypical epithelial cells and necrosis. Histologically, the mucosal and crypt epithelium was moderately hyperplastic with a loss of goblet cells, increased mitoses, and frequent crypt abscesses. Within the lamina propria and extending into the submucosa was a marked neutrophilic infiltrate, with low numbers of lymphocytes, histiocytes, plasma cells, and eosinophils. The histologic diagnosis was chronic, diffuse, marked suppurative and lymphocytic ileitis. Warthin-Starry silver staining of the ileal biopsy and imprint specimens demonstrated numerous pleomorphic, curved bacilli consistent with Lawsonia intracellularis. Polymerase chain reaction (PCR) and immunohistochemistry confirmed the identity of the infectious agent. L intracellularis infection may be underdiagnosed because silver stain is required to visualize the organism with light microscopy and because the pathognomonic crypt hyperplasia may be complicated by secondary pathologic changes. Application of silver stain to cytologic specimens should be considered when distal intestinal lesions associated with hyperplastic epithelium, with or without inflammation, hemorrhage, or necrosis, are identified in animals with clinical signs of enteritis, especially in frequently affected species or in stressed or young animals.

Animals↗
PubMed2006

STAT3 activation via interleukin 6 trans-signalling contributes to ileitis in SAMP1/Yit mice.

BACKGROUND AND AIMS: SAMP1/Yit mice spontaneously develops intestinal inflammation. Previously, we demonstrated that the signal transducer and activator of transcription (STAT)-3/suppressor of cytokine signalling (SOCS)-3 pathway is pivotal in human inflammatory bowel disease. In our studies in SAMP1/Yit mice, the aim was to investigate whether STAT3 activation contributes to ileitis and to examine the therapeutic effects of this signal blockade. METHODS: Intestinal expression of phospho-STAT3 in SAMP1/Yit mice and control AKR/J mice was examined by western blotting and immunohistochemistry. SOCS3 and interleukin 6 (IL-6) mRNA were determined by northern blotting and reverse transcription-polymerase chain reaction, respectively. We also examined the effects of intravenously injected hyper-IL-6, an IL-6/soluble IL-6 receptor fusion protein, and of soluble gp130-Fc, a specific inhibitor of soluble IL-6 receptor signalling, on STAT3 phosphorylation and disease severity in SAMP1/Yit mice. RESULTS: Phospho-STAT3 was expressed strongly during the disease course in SAMP1/Yit mice but only transiently in AKR/J mice. Phospho-STAT3 was localised to epithelial and mononuclear cells in the diseased intestine of SAMP1/Yit mice. SOCS3 as well as IL-6 mRNAs were expressed in affected intestine. Administration of hyper-IL-6 caused disease exacerbation and enhancement of STAT3 phosphorylation. In contrast, soluble gp130-Fc administration ameliorated the disease and suppressed STAT3 phosphorylation. CONCLUSION: STAT3 signalling is critical in the development of intestinal inflammation in SAMP1/Yit mice. Blockade of this signalling pathway by soluble gp130-Fc may have therapeutic effects in inflammatory bowel disease.

Animals↗
PubMed1995

Duration of recurrent ileitis after ileocolonic resection correlates with presurgical extent of Crohn's disease.

Crohn's disease of the terminal ileum recurs in a predictable sequence proximal to the ileocolonic anastomosis after surgical resection. To confirm the suspicion that the duration of recurrent ileitis correlates with the extent of presurgical disease, this study investigated 23 consecutive patients with recurrent Crohn's disease symptoms who had undergone ileocaecal resections between 1982 and 1992 at our institution and had both preoperative and postoperative small bowel follow through studies available for comparison. All films were reviewed by a blinded gastrointestinal radiologist using uniform criteria. Symptomatic recurrence was reported at a mean (SEM) of 29 (25) months after resection. Presurgical length of inflammation averaged 26 (15) (8-57) cm and at recurrence 24 (14) (7-55) cm. The correlation coefficient (r) between pre and postsurgical extent of ileal disease was 0.70 (p < 0.0001). Seven patients had sequential small bowel series after 20 (10) (7-36) months without intervening surgery. The extent of measured inflammation between examinations correlated with r = 0.995 (p < 0.0001), showing the consistency of the measurement process. The close correlation between the duration of postoperative recurrence with the extent of presurgical disease is another example of individual patterns of recurrent Crohn's disease and is an additional factor to be considered when contemplating surgical resections.

Adolescent↗
PubMed1987

Ileal carcinoma and tuberculous ileitis.

A 76 year old woman presented with abdominal pain and weight loss. At laparotomy she was found to have an adenocarcinoma of the ileum arising in a segment of tuberculous ileitis. The possible significance of this association is discussed.

Adenocarcinoma↗
PubMed1995

Na(+)-K(+)-ATPase alpha 1- and beta 1-mRNA and protein levels in rat small intestine in experimental ileitis.

Na(+)-K(+)-adenosinetriphosphatase (ATPase) plays a key role in the absorption of electrolytes, water, and nutrients from the small intestine. The expression of Na(+)-K(+)-ATPase was examined in isolated enterocytes during the course of the ileal inflammatory response elicited by intraluminal administration of 2,4,6-trinitrobenzenesulfonic acid. The ileal inflammatory response was characterized by a marked cellular infiltrate, villous atrophy, and crypt hyperplasia along with fibrosis and smooth muscle hypertrophy. Peak levels of myeloperoxidase were observed at day 7, and ileal mucosal injury was paralleled by increases in ileal mucosal permeability. Ileal enterocytes were harvested from days 3 to 30 after the induction of ileitis. Decreases in Na(+)-K(+)-ATPase functional activity were observed from days 3 to 21 and were accompanied by corresponding decreases in Na(+)-K(+)-ATPase pump abundance, alpha 1- and beta 1-protein expression, and mRNA abundance, whereas Na(+)-K(+)-ATPase turnover, Michaelis-Menten constant values, and inhibition constant values for Na+ and ouabain, respectively, were unaltered. Alterations in transcriptional and posttranscriptional events may determine the changes in Na(+)-K(+)-ATPase activity in this particular model. Additionally observed increases in thymidine kinase and ornithine decarboxylase activities appear to signify alterations in the state of differentiation of the ileal epithelium and may determine the phenotypic expression of enterocyte transporters and permeability in the setting of inflammation.

Animals↗
PubMed2001

Th1-type responses mediate spontaneous ileitis in a novel murine model of Crohn's disease.

We describe here the immunologic characterization of a new mouse strain, SAMP1/Yit, which spontaneously develops a chronic intestinal inflammation localized to the terminal ileum. The resulting ileitis bears a remarkable resemblance to human Crohn's disease. This strain of mice develops discontinuous, transmural inflammatory lesions in the terminal ileum with 100% penetrance by 30 weeks of age. The intestinal inflammation is characterized by massive infiltration of activated CD4+ and CD8alpha(+)TCRalphabeta(+) T cells into the lamina propria and is accompanied by a dramatic decrease in the intraepithelial lymphocyte CD8alpha(+)TCRgammadelta(+)/CD8alpha(+)TCRalphabeta(+) ratio. The results of adoptive transfer experiments strongly suggest that CD4+ T cells that produce a Th1-like profile of cytokines, e.g., IFN-gamma and TNF, mediate the intestinal inflammation found in SAMP1/Yit mice. In addition, pretreatment of adoptive transfer recipients with a neutralizing anti-TNF antibody prevents the development of intestinal inflammation, suggesting that TNF plays an important role in the pathogenesis of intestinal inflammation in this model. To our knowledge, these data provide the first direct evidence that Th1-producing T cells mediate intestinal inflammation in a spontaneous animal model of human Crohn's disease.

Adoptive Transfer↗
PubMed2006

Contemporary morphologic definition of backwash ileitis in ulcerative colitis and features that distinguish it from Crohn disease.

Terminal ileum (TI) sections from 250 ulcerative colitis (UC) total colectomy specimens resected during 3 periods and endoscopic TI biopsy specimens from 100 contemporary chronic UC and 100 Crohn disease (CD) patients were reviewed. The respective proportions of cases resected during the 3 periods with moderately or markedly active cecal UC were 72%, 34%, and 2% and with moderate or marked backwash ileitis (BWI), 21%, 18%, and 0%. The activity level of BWI correlated with level of cecal UC. In contemporary initial endoscopic TI biopsy specimens, 6% of chronic UC patients had BWI, all with moderately to markedly active cecal chronic UC. In CD cases, 75% had chronic or active enteritis, consisting of patchy lamina propria edema containing mildly active inflammation, crypt disarray, and focally blunted or flattened villi. Mucous gland metaplasia was present in 27% of CD biopsy specimens. BWI should be restricted to active enteritis that involves the ileum in a contiguous pattern from the cecum that has a similar or greater degree of active inflammation. Mild BWI predominantly involves the superficial mucosa in a contiguous pattern. Focal isolated ileal erosions, mucous gland metaplasia, or patchy edema with mild active inflammation are features of CD.

Biopsy↗
PubMed1976

Terminal ileitis, mesenteric lymphadenitis and appendicitis due to Yersinia pseudotuberculosis type VA: case report.

A case of terminal ileitis, mesenteric lymphadenitis and appendicitis is reported. Serological studies indicated infection with Yersinia pseudotuberculosis type VA. The patient's illness ran a chronic course necessitating resection of the terminal ileum. Histological examination of the appendix and a mesenteric lymph node in the acute stage revealed granulomas with central necrosis. This is the first human case in which the subtype VA has been identified.

Adult↗