Supplementation with organic yeast-derived selenium provides immune protection against experimental necrotic enteritis in broiler chickens.

Necrotic enteritis (NE) is a potentially fatal poultry disease that causes enormous economic losses in the poultry industry worldwide. The study aimed to evaluate the effects of dietary organic yeast-derived selenium (Se) on immune protection against experimental necrotic enteritis (NE) in commercial broilers. Chickens were fed basal diets supplemented with different Se levels (0.25, 0.50, and 1.00 Se mg/kg). To induce NE, Clostridium perfringens (C. perfringens) was orally administered at 14 days of age post hatch. The results showed that birds fed 0.25 Se mg/kg exhibited significantly increased body weight gain compared with the non-supplemented/infected birds. There were no significant differences in gut lesions between the Se-supplemented groups and the non-supplemented group. The antibody levels against α-toxin and NetB toxin increased with the increase between 0.25 Se mg/kg and 0.50 Se mg/kg. In the jejunal scrapings and spleen, the Se-supplementation groups up-regulated the transcripts for pro-inflammatory cytokines IL-1ß, IL-6, IL-8, iNOS, and LITAF and avian ß-defensin 6, 8, and 13 (AvBD6, 8 and 13). In conclusion, supplementation with organic yeast-derived Se alleviates the negative consequences and provides beneficial protection against experimental NE.

Extracellular adenosine triphosphate skews the T helper cell balance and enhances neutrophil activation in mice with food allergies.

Exposure to food allergens elicits fast changes in the intestinal microenvironment, which guides the development of allergic reactions. Investigating the key information about these changes may help in better understanding food allergies. In this research, we explored the relationship between a food allergy and extracellular adenosine triphosphate (ATP), a danger molecule that has been proved to regulate the onset of allergic asthma and dermatitis but has not been studied in food allergies, by developing a unique animal model through allergen-containing diet feeding. After consuming an allergen-containing diet for 7 days, the allergic mice exhibited severe enteritis with elevated luminal ATP levels. The dysregulated luminal ATP worsened food-induced enteritis by enhancing Th17 cell responses and increasing mucosal neutrophil accumulation. In vitro experiments demonstrated that ATP intervention facilitated Th17 cell differentiation and neutrophil activation. In addition, the diet-induced allergy showed noticeable gut dysbiosis, characterized by decreased microbial diversity and increased diet-specific microbiota signatures. As the first, we show that food-induced enteritis is associated with an elevated concentration of luminal ATP. The dysregulated extracellular ATP exacerbated the enteritis of mice to a food challenge by manipulating intestinal Th17 cells and neutrophils.

Minimally Invasive Approaches to Diagnose and Monitor Eosinophilic GI Diseases.

PURPOSE OF REVIEW: This review seeks to understand novel avenues for eosinophilic GI disease management. Biomarkers offer a unique and non-invasive approach to tracking EoE disease progression. While no biomarkers have definitively met the diagnostic criteria for eosinophilic GI diseases, some biomarkers have been shown to be associated with disease activity. Here, we examine the potential of recently studied biomarkers. RECENT FINDINGS: Current research shows advancements in blood, luminal fluid, and breath testing. Particular areas of interest include mRNA analyses, protein fingerprinting, amplicon sequence variants (ASVs), T cells and IgE receptors, eosinophilic cationic proteins, cytokines, and nitric oxide exhalation. Preliminary results showed that mucosal biomarkers, directly captured from the esophagus, may reflect the best representation of biopsy-based results, in contrast to biomarkers obtained from indirect or peripheral (blood, breath) methods. However, this is based on limited clinical studies without sufficient numbers to evaluate true diagnostic accuracy. Large-scale randomized trials are needed to fully ascertain both the optimal sampling technique and the specific biomarkers that reflect diagnostic status of the disease.

Severe Immune-Related Enteritis after In Utero Exposure to Pembrolizumab.

Immune checkpoint blockade has become standard treatment for many types of cancer. Such therapy is indicated most often in patients with advanced or metastatic disease but has been increasingly used as adjuvant therapy in those with early-stage disease. Adverse events include immune-related organ inflammation resembling autoimmune diseases. We describe a case of severe immune-related gastroenterocolitis in a 4-month-old infant who presented with intractable diarrhea and failure to thrive after in utero exposure to pembrolizumab. Known causes of the symptoms were ruled out, and the diagnosis of pembrolizumab-induced immune-related gastroenterocolitis was supported by the results of histopathological assays, immunophenotyping, and analysis of the level of antibodies against programmed cell death protein 1 (PD-1). The infant's condition was successfully treated with prednisolone and infliximab.

Trans Fatty Acid Intake Induces Intestinal Inflammation and Impaired Glucose Tolerance.

Background and Aims: Many nutritional and epidemiological studies have shown that high consumption of trans fatty acids can cause several adverse effects on human health, including cardiovascular disease, diabetes, and cancer. In the present study, we investigated the effect of trans fatty acids on innate immunity in the gut by observing mice fed with a diet high in trans fatty acids, which have been reported to cause dysbiosis. Methods: We used C57BL6/J mice and fed them with normal diet (ND) or high-fat, high-sucrose diet (HFHSD) or high-trans fatty acid, high-sucrose diet (HTHSD) for 12 weeks. 16S rRNA gene sequencing was performed on the mice stool samples, in addition to flow cytometry, real-time PCR, and lipidomics analysis of the mice serum and liver samples. RAW264.7 cells were used for the in vitro studies. Results: Mice fed with HTHSD displayed significantly higher blood glucose levels and advanced fatty liver and intestinal inflammation, as compared to mice fed with HFHSD. Furthermore, compared to mice fed with HFHSD, mice fed with HTHSD displayed a significant elevation in the expression of CD36 in the small intestine, along with a reduction in the expression of IL-22. Furthermore, there was a significant increase in the populations of ILC1s and T-bet-positive ILC3s in the lamina propria in mice fed with HTHSD. Finally, the relative abundance of the family Desulfovibrionaceae, which belongs to the phylum Proteobacteria, was significantly higher in mice fed with HFHSD or HTHSD, than in mice fed with ND; between the HFHSD and HTHSD groups, the abundance was slightly higher in the HTHSD group. Conclusions: This study revealed that compared to saturated fatty acid intake, trans fatty acid intake significantly exacerbated metabolic diseases such as diabetes and fatty liver.

Eosinophilic colitis: an infrequent disease with difficult diagnose.

Eosinophilic colitis (EC) is a rare entity. It is part of eosinophilic gastroenteritis, a rare inflammatory disorder characterised by eosinophilic infiltration of tissues that can affect any segment of the digestive tract. The diagnosis is established by the presence of an increased eosinophilic infiltrate in the colon wall in symptomatic patients. There is no characteristic clinical picture of EC. It can be associated with abdominal pain, changes in bowel movements, diarrhoea and rectal bleeding. Biopsies are mandatory if EC is suspected and despite visualising a normal mucosa. Although there are no protocol guidelines in this regard, steroid treatment is the first option in controlling the disease. Increasing the knowledge of clinicians and pathologists of this disorder and the recording its real incidence and population impact, could improve the understanding and treatment of the disease.

Integrative Transcriptomic and Small RNA Sequencing Reveals Immune-Related miRNA-mRNA Regulation Network for Soybean Meal-Induced Enteritis in Hybrid Grouper, Epinephelus fuscoguttatus♀ × Epinephelus lanceolatus♂.

A 10-week feeding experiment was conducted to reveal the immune mechanism for soybean meal-induced enteritis (SBMIE) in hybrid grouper, Epinephelus fuscoguttatus ♀ × Epinephelus lanceolatus ♂. Four isonitrogenous and isolipidic diets were formulated by replacing 0, 10, 30, and 50% fish meal protein with soybean meal (namely FM, SBM10, SBM30, and SBM50, respectively). The weight gain rate of the SBM50 group was significantly lower than those of the other groups. Plica height, muscular layer thickness, and goblet cells of the distal intestine in the SBM50 group were much lower than those in the FM group. The intestinal transcriptomic data, including the transcriptome and miRNAome, showed that a total of 6,390 differentially expressed genes (DEGs) and 92 DEmiRNAs were identified in the SBM50 and FM groups. DEmiRNAs (10 known and 1 novel miRNAs) and their DE target genes were involved in immune-related phagosome, natural killer cell-mediated cytotoxicity, Fc gamma R-mediated phagocytosis, and the intestinal immune network for IgA production pathways. Our study is the first to offer transcriptomic and small RNA profiling for SBMIE in hybrid grouper. Our findings offer important insights for the understanding of the RNA profile and further elucidation of the underlying molecular immune mechanism for SBMIE in carnivorous fish.

Patients with radiation enteritis present regulatory T cell impairment associated with CTLA-4.

Radiation enteritis is one of the most common side effects of ionizing radiation in patients with pelvic cancers. Increasing amounts of evidence indicate that pro-inflammatory responses significantly contribute to the development of radiation enteritis. In this study, we investigated the association between T regulatory (Treg) cells and the risk of developing radiation enteritis in cervical cancer patients. The following observations were made. First, the frequencies of CD25hiFoxp3+ Treg cells were significantly lower in patients with radiation enteritis than in both healthy subjects and cervical cancer patients without radiation enteritis. Also, patients with the more severe grade 3 enteritis presented significantly lower Treg levels than patients with the more common grade 1 enteritis. Second, the expression of several molecules associated with Treg function, including CTLA-4, IL-10, TGF-ß, and perforin, was significantly lower in patients with radiation enteritis than in healthy subjects. In patients without radiation enteritis, however, only CTLA-4, but not other Treg-associated suppressive molecules, was reduced in Treg cells. Third, Treg cells can markedly suppress CD8 T cell proliferation, but in patients with radiation enteritis, this function of Treg cells was significantly impaired, in a manner that was associated with lower CTLA-4 expression. Overall, these data suggest that the frequency and function of Treg cells is negatively associated with the risk of developing enteritis following radiation. In clinical practice, the characteristics of Treg cells may be considered to evaluate the risk of developing enteritis if the cancer patient is receiving ionizing radiation.

Low lethal doses of Streptococcus iniae caused enteritis in Siberian sturgeon (Acipenser baerii).

In aquaculture, the incidence of enteritis due to Streptococcus iniae infection in Siberian sturgeon (Acipenser baerii) has increased in recent years. The pathogenesis of S. iniae is largely unknown due to the paucity of experimental studies on fish intestinal inflammation. In this study, S. iniae infection of A. baerii juveniles was induced by anal intubation of 0.15 mL at a low lethal dose (2 × 107 CFU/mL). Intestinal pathology and gene expression studies were conducted within 10 days of the experiment. Histopathological examination showed severe intestinal lesions, inflammatory cell infiltration, intestinal submucosa edema, epithelial cell shedding and necrosis. Predominant symptoms of exudative inflammation, metamorphic inflammation and proliferative inflammation on days 1-3, 4-6, and 7-10 post infection were shown, respectively. Ultrastructural observations also revealed fractured microvilli and shedding on days 4-6. Intestinal villi gradually repaired during the subsequent 7-10 days post infection. Expression of the pro-inflammatory cytokines, tumor necrosis factor and interleukin 1ß were up-regulated on days 1-3 followed by a significant decrease on day 5, ultimately reaching control levels on day 10 post infection. A similar pattern was shown in mucus cells, involving mucin secretion and expression of the mucin encoding gene, Mucin-2. These results showed the cellular response to S. iniae infection associated with inflammatory genes expression in the Siberian sturgeon.

Edwardsiella tarda induces enteritis in farmed seahorses (Hippocampus erectus): An experimental model and its evaluation.

Bacterial enteritis is an important deadly threat to farmed seahorses. However, its pathogenesis is obscure because of the paucity of reproducible experimental intestinal inflammation models. Herein, a strain of Edwardsiella tarda YT1 from farmed seahorse Hippocampus erectus was isolated and identified by morphological, phylogenetic, and biochemical analysis, and confirmed as a pathogen of enteritis for the first time by challenge experiment. Two E. tarda concentrations (1 × 105 and 1 × 107 colony forming units [cfu] ml-1) were confirmed suitable for an enteritis model by intraperitoneal injection. To develop and evaluate the experimental model, we challenged seahorses with E. tarda and found that (1) the infection inhibited body length increase, significantly decreased body weight (P < 0.05), and induced typical pathological features including anorexia, anal inflammation, and intestinal fluid retention; (2) 19 external (weight, height, anal inflammation, feeding status, and intestinal fluid retention), histological (goblet and inflammatory cell numbers and thickening of lamina propria and muscularis mucosae), and molecular (hepcidin, liver-expressed antimicrobial peptide, lysozyme, piscidin, interleukin [IL]-1ß, IL-1ß receptor, IL-2, IL-10, interferon1, tumor necrosis factor [TNF]-α, and toll-like receptor 5 [TLR5]) indicators were suitable for model evaluation, as they could sensitively respond and varied similarly throughout the experiment, indicating the high sensitivity of seahorses against pathogen invasion; (3) TLR5 may play an essential role in triggering host immune responses during E. tarda-induced chronic enteritis, and (4) the evaluating system could reflect the pattern and intensity of disease progression. Thus, we developed an experimental model and an evaluating system of bacterial enteritis in farmed seahorses, helping us to reveal the pathogenesis of bacterial enteritis, identify potential therapeutic drugs, and search suitable genetic markers for seahorse molecular breeding.

Eosinophilic Gastrointestinal Diseases in Children: A Practical Review.

Primary eosinophilic gastrointestinal diseases (EGIDs) represent a heterogeneous group of disorders characterized by eosinophilic inflammation in the absence of known causes for eosinophilia, selectively affecting different segments of the gastrointestinal tract. While pediatric eosinophilic esophagitis (EoE) is a well-defined disease with established guidelines, Eosinophilic Gastritis (EoG), Eosinophilic Gastroenteritis (EoGE) and Eosinophilic Colitis (EoC) remain a clinical enigma with evidence based on limited anecdotal case reports. Large cross-sectional studies in the US defined a prevalence of EoG and EoGE ranging from 1,5 to 6,4/100.000 and from 2,7 to 8,3/100.000 subjects respectively, while the prevalence of EoC ranges from 1,7 to 3,5/100.000 subjects. Regarding the pathogenesis, it is hypothesized that EGIDs result from the interplay between genetic predisposition, intestinal dysbiosis and environmental triggers. Clinically, EGIDs might present with different and nonspecific gastrointestinal symptoms depending on the involved intestinal tract and the extension of eosinophilic inflammatory infiltrate. The diagnosis of EGIDs requires: 1. recurrent gastrointestinal symptoms, 2. increased eosinophils for high power field in biopsy specimens, 3. absence of secondary causes of gastrointestinal eosinophilia. No validated guidelines are available on the clinical management of patients with EGIDs. Evidence from case reports and small uncontrolled case series suggests the use of dietary and corticosteroids as the first-line treatments. Considering the clinical follow-up of EGIDs, three different patterns of disease course are identified: single flare, recurring course-disease and chronic course-disease. This review will focus on pediatric EGIDs distal to esophagus, including Eosinophilic Gastritis (EoG), Eosinophilic Gastroenteritis (EoGE) and Eosinophilic Colitis (EoC).

Molecular, endoscopic, histologic, and circulating biomarker-based diagnosis of eosinophilic gastritis: Multi-site study.

BACKGROUND: Eosinophilic gastritis (EG) is a clinicopathologic disorder with marked gastric eosinophilia and clinical symptoms. There is an unmet need among patients with EG for more precise diagnostic tools. OBJECTIVE: We aimed to develop tissue- and blood-based diagnostic platforms for EG. METHODS: Patients with EG and control subjects without EG were enrolled across 9 Consortium of Eosinophilic Gastrointestinal Disease Researchers-associated sites. An EG Diagnostic Panel (EGDP; gastric transcript subset) and EG blood biomarker panel (protein multiplex array) were analyzed. EGDP18 scores were derived from the expression of 18 highly dysregulated genes, and blood EG scores were derived from dysregulated cytokine/chemokine levels. RESULTS: Gastric biopsy specimens and blood samples from 185 subjects (patients with EG, n = 74; control subjects without EG, n = 111) were analyzed. The EGDP (1) identified patients with active EG (P < .0001, area under the curve ≥ 0.95), (2) effectively monitored disease activity in longitudinal samples (P = .0078), (3) highly correlated in same-patient samples (antrum vs body, r = 0.85, P < .0001), and (4) inversely correlated with gastric peak eosinophil levels (r = -0.83, P < .0001), periglandular circumferential collars (r = -0.73, P < .0001), and endoscopic nodularity (r = -0.45, P < .0001). For blood-based platforms, eotaxin-3, thymus and activation-regulated chemokine, IL-5, and thymic stromal lymphopoietin levels were significantly increased. Blood EG scores (1) distinguished patients with EG from control subjects without EG (P < .0001, area under the curve ≥ 0.91), (2) correlated with gastric eosinophil levels (plasma: r = 0.72, P = .0002; serum: r = 0.54, P = .0015), and (3) inversely correlated with EGDP18 scores (plasma: r = -0.64, P = .0015; serum: r = -0.46, P = .0084). Plasma eotaxin-3 levels strongly associated with gastric CCL26 expression (r = 0.81, P < .0001). CONCLUSION: We developed tissue- and blood-based platforms for assessment of EG and uncovered robust associations between specific gastric molecular profiles and histologic and endoscopic features, providing insight and clinical readiness tools for this emerging rare disease.

Eosinophilic Gastroenteritis: Clinical Manifestation, Natural Course, and Evaluation of Treatment with Corticosteroids and Vedolizumab.

BACKGROUND: Eosinophilic gastroenteritis (EGE) is a rare, chronic inflammatory condition of the gastrointestinal tract. Little is known about its natural history and treatment outcomes. The aims of our analysis were to describe clinical presentation, response to current medical treatments, and to evaluate the response of refractory EGE to anti-integrin therapy. METHODS: Patients with confirmed diagnosis of EGE fulfilling the diagnostic criteria: (1) the presence of gastrointestinal symptoms, (2) dense eosinophilic infiltration of the gastrointestinal mucosa, and (3) exclusion of other conditions leading to gastrointestinal eosinophilia were included in this analysis. In patients non-responding to corticosteroids and/or anti-TNF treatment the integrin blocker vedolizumab was used. RESULTS: EGE patients (n = 22) were predominantly female (63%) with a median age at diagnosis of 41.5 years. The most frequent symptoms were abdominal pain (100%), diarrhea (59%), nausea/vomiting (36%), and bloating (27%). No pathognomonic endoscopic alterations were found. Eosinophilic infiltration was observed in the majority of patients in more than one segment. Patients were treated with systemic steroids, topical, and enteral release steroids in 21/22 (95%) patients, proton pump inhibitors in 7/22 (32%), TNFα inhibitors in 3/22 (14%), and vedolizumab in 4/22 (18%) patients. In 3/4 of steroid-refractory patients vedolizumab induced a clinical and histological improvement. CONCLUSIONS: The combination of highly variable clinical presentation, subtle endoscopic abnormalities, and involvement of several GI segments undermines the difficulty to diagnose EGE and the need for structured biopsy sampling. Corticosteroids were efficient in the majority of patients to induce remission. Response to the integrin blocker vedolizumab suggests further assessment in refractory cases.

Corn gluten meal induces enteritis and decreases intestinal immunity and antioxidant capacity in turbot (Scophthalmus maximus) at high supplementation levels.

Corn gluten meal (CGM) is an important alternative protein source in aquafeed production. However, in turbot (Scophthalmus maximus), CGM could not be effectively utilized because of its low digestibility, the reason for which is still unclear. The purpose of the present study was to investigate and elucidate the cause for the poor utilization of CGM by turbot from the view of gut health. An 8-week feeding trial was conducted with turbot individuals (initial body weight 11.4 ± 0.2 g), which were fed with one of four isonitrogenous and isolipidic diets formulated to include 0%, 21.2%, 31.8%, and 42.6% CGM to progressively replace 0%, 33%, 50%, and 67% fish meal (FM) protein in a FM-based diet, respectively. The results showed that CGM caused dose-dependent decreases in (1) growth performance, nutrient digestibility, and feed utilization; (2) activities of brush-border membrane enzymes; (3) intestinal antioxidant indices of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase activities, and reduced glutathione level; (4) intestinal immune parameters of acid phosphatase activity, complement 3, complement 4, and IgM concentrations. Dose-dependent increases in the severity of the inflammation, with concomitant alterations on microvilli structure and increasing expression of inflammatory cytokine genes of Il-1ß, Il-8, and Tnf-α were observed but without a change in the intracellular junctions and the epithelial permeability established by the plasma diamine oxidase activity and D-lactate level examinations. In conclusion, the present work proved that CGM negatively affected the gut health of turbot by inducing enteritis and by decreasing intestinal immunity and antioxidant capacity, which could be one of the reasons for the reduced utilization of CGM by turbot.

N-acetylcysteine modulates lipopolysaccharide-induced intestinal dysfunction.

The gastrointestinal epithelium functions in nutrient absorption and pathogens barrier and its dysfunction directly affects livestock performance. N-Acetylcysteine (NAC) improves mucosal function, but its effects on intestinal functions at the molecular level remain unclear. Here, we performed gene expression profiling of the pig small intestine after dietary NAC treatment under LPS challenge and investigated the effects of NAC on intestinal epithelial cells in vitro. Dietary NAC supplementation under LPS challenge altered the small intestine expression of 959 genes related to immune response, inflammatory response, oxidation-reduction process, cytokine-cytokine receptor interaction, and the cytokine-mediated signalling, Toll-like receptor signalling pathway, Jak-STAT signalling pathway, and TNF signalling pathway. We then analysed the expression patterns of the top 10 altered genes, and found that NAC markedly stimulated HMGCS3 and LDHC expression in IPEC-J2 cells. In vitro, NAC pre-treatment significantly reduced TNF-α and NF-κB, TNF-α, IFN-γ, and IL-6 expression in LPS-induced IPEC-J2 cells. NAC treatment also significantly reduced oxidative stress in LPS-induced IPEC-J2 cells and alleviated intestinal barrier function and wound healing. Thus, NAC as a feed additive can enhance livestock intestinal health by modulating intestinal inflammation, permeability, and wound healing under LPS-induced dysfunction, improving our molecular understanding of the effects of NAC on the intestine.

Predictivity of Autoimmune Stigmata for Gluten Sensitivity in Subjects with Microscopic Enteritis: A Retrospective Study.

Non-celiac gluten sensitivity (NCGS) is an emerging gluten-related condition. We investigated whether the presence of autoimmune stigmata in a group of patients with clinical suspicion of NCGS and a histological picture of microscopic enteritis (ME) could be a predictive factor of NCGS. Patients with ME were followed up by periodical examinations. At baseline, we collected data about previous clinical history, including autoimmune diseases. NCGS was diagnosed according to Salerno criteria; other causes of ME were diagnosed according to well-established protocols. Patients with celiac disease were excluded. Student's and chi-square tests were used in univariate analysis. Kaplan-Meier curves and Cox regression were used to estimate hazard ratios (HR). Sixty-three patients were included. Twenty-two had a final diagnosis of NCGS; the remaining 41 had non-gluten-related causes of ME. Prevalence of autoimmune thyroiditis was higher among NCGS patients (40.1%) than in other ME (14.6%; p = 0.03). NCGS showed higher positivity rate for anti-gliadin (27.3% versus 2.5%; p = 0.006) and anti-nucleus (45.4% versus 12.2%; p = 0.005). Autoimmune thyroiditis had a non-significant trend (p = 0.06) for NCGS diagnosis, (HR = 2.4). Both anti-gliadin (HR = 2.4; p = 0.04) and anti-nucleus (HR = 2.7; p = 0.04) were directly associated with NCGS diagnosis. In conclusion, NCGS may have a cohort of autoimmune stigmata that can precede its diagnosis.

[The clinical characteristics of immunocompetent adults with chronic active Epstein-Barr virus associated enteritis].

Objective: To investigate the clinical and pathological characteristics of chronic active Epstein-Barr virus associated enteritis (CAEAE) . Methods: The clinical data of 6 CAEAE patients in Peking Union Medical College Hospital were retrospectively analyzed from January 2010 to November 2017, including clinical manifestations, endoscopic, pathological features, medications and clinical outcome. Results: The male∶female ratio was 4∶2 and the average age was 34 years old. All patients did not have personal and family history of immunodeficiency. The common symptoms consisted of fever (6/6), abdominal pain (6/6), hematochezia (6/6) and diarrhea (5/6). The most frequently affected sites were colorectum (5/6), followed by small intestine (3/6). Further serologic tests revealed a high load of serum Epstein-Barr virus(EBV) DNA. The main manifestations under endoscopy were multifocal or diffuse irregular ulcers. There was inflammation in the ulcer bases and surrounding areas, where EBV-encoded small RNA (EBER) was positive by in situ hybridization (6/6). The common complications were massive hemorrhage (3/6) and intestinal perforation (2/6). None of treatment agents including glucocorticoid, ganciclovir, foscarnet sodium and cytotoxic drugs was effective. All patients died within 0.5 to 13 months after diagnosis. Conclusions: CAEAE in immunocompetent individuals is a rare disorder with poor prognosis. It is difficult to differentiate CAEAE from inflammatory bowel disease due to similar clinical and endoscopic manifestations.