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Patients with eosinophilic gastritis, duodenitis, or both conditions were randomly assigned to receive placebo or AK002, an anti–Siglec-8 antibody that depletes eosinophils and inhibits mast cells. AK002 reduced eosinophils and symptoms, with frequencies of adverse events similar to placebo, although infusion-related reactions were more common with AK002.

Eosinophilic gastritis (EG), defined by histological criteria as marked eosinophilia in the stomach, is rare, and large studies in children are lacking. We sought to describe the clinical, endoscopic, and histopathological features of EG, assess for any concurrent eosinophilia at other sites of the gastrointestinal (GI) tract, and evaluate response to dietary and pharmacological therapies. Pathology files at our medical center were searched for histological eosinophilic gastritis (HEG) with ≥70 gastric eosinophils per high-power field in children from 2005 to 2011. Pathology slides were evaluated for concurrent eosinophilia in the esophagus, duodenum, and colon. Medical records were reviewed for demographic characteristics, symptoms, endoscopic findings, comorbidities, and response to therapy. Thirty children with severe gastric eosinophilia were identified, median age 7.5 years, 14 of whom had both eosinophilia limited to the stomach and clinical symptoms, fulfilling the clinicopathological definition of EG. Symptoms and endoscopic features were highly variable. History of atopy and food allergies was common. A total of 22% had protein-losing enteropathy (PLE). Gastric eosinophilia was limited to the fundus in two patients. Many patients had associated eosinophilic esophagitis (EoE, 43%) and 21% had eosinophilic enteritis. Response to dietary restriction therapy was high (82% clinical response and 78% histological response). Six out of sixteen patients had persistent EoE despite resolution of their gastric eosinophilia; two children with persistent HEG post therapy developed de novo concurrent EoE. HEG in children can be present in the antrum and/or fundus. Symptoms and endoscopic findings vary, highlighting the importance of biopsies for diagnosis. HEG is associated with PLE, and with eosinophilia elsewhere in the GI tract including the esophagus. The disease is highly responsive to dietary restriction therapies in children, implicating an allergic etiology. Associated EoE is more resistant to therapy.

Eosinophilic esophagitis is an immune-mediated, chronic, inflammatory disease of the esophagus that was first recognized as a distinct entity less than three decades ago. 1 The immunopathogenesis of the disease is characterized by type 2 helper T (Th2)–cell inflammation involving T cells, eosinophils, mast cells, and the cytokines interleukin-4, interleukin-5, interleukin-13, and thymic stromal lymphopoietin. 2 These cells and mediators are potential targets for antiinflammatory medications. The prevalence of eosinophilic esophagitis has increased rapidly. In Western countries, the disease currently affects approximately 1 in 3000 persons. 3 The most common symptom of eosinophilic esophagitis in adults is dysphagia with solid food intake, often . . .

Radiation enteritis is the most common and serious complication of abdominal or pelvic radiation therapy. Mesenchymal stem cells (MSCs), as well as cell protection agents, inhibit apoptosis and promote the proliferation of injured tissues. 3 human umbilical cords MSCs (UCMSCs) were injected into the tail vein or peritoneal cavity of a rat model of radiation enteritis. The temporary protective effect was assessed by identification of donor cells, detection of cellular immune parameters and inflammatory cytokine levels, quantitation of jejunum mucosal preservation and examination of the rat remaining life. Only the rats in the intraperitoneal injection group exhibited a few positive donor cells 7 days after transplantation. CD4 +/CD8 + T cells, a cellular immune parameter, decreased in the abdominal exudate of intraperitoneal injection group, compared with the model-only control and tail vein groups (both P < .05). Both serum and abdominal exudate TNF-α and IL-6 levels in the intraperitoneally injected rats rapidly decreased and were significantly different from those in the model-only control and tail vein injection groups (all P < .05). Mucosal surface area and survival time increased in the intraperitoneal injection group compared with the vehicle and tail vein injection groups (all P = .000). Therefore, the administration of UCMSCs with intraperitoneal injection approach postponed death in a rat model of radiation enteritis, which was associated with reduced serum levels of proinflammatory cytokines (TNF-α, IL-6). However, UCMSCs injected via the tail vein triggered an intense cellular immune response in the serum that adversely affects their survival. This treatment failed to suppress circulating serum and abdominal exudate levels of TNF-α and IL-6 and could not provide a therapeutic benefit for prolonging life against acute radiation enteritis.

Eosinophilic gastrointestinal disorders (EGID) are a group of disorders characterized by pathologic eosinophilic infiltration of the esophagus, stomach, small intestine, or colon leading to organ dysfunction and clinical symptoms (J Pediatr Gastroenterol Nutr; Spergel et al., 52: 300–306, 2011). These disorders include eosinophilic esophagitis (EoE), eosinophilic gastritis (EG), eosinophilic gastroenteritis (EGE), eosinophilic enteritis (EE), and eosinophilic colitis (EC). Symptoms are dependent not only on the location (organ) as well as extent (layer invasion of the bowel wall). Common symptoms of EoE include dysphagia and food impaction in adults and heartburn, abdominal pain, and vomiting in children. Common symptoms of the other EGIDs include abdominal pain, nausea, vomiting, early satiety, diarrhea, and weight loss. These disorders are considered immune-mediated chronic inflammatory disorders with strong links to food allergen triggers. Treatment strategies focus on either medical or dietary therapy. These options include not only controlling symptoms and bowel inflammation but also on identifying potential food triggers. This chapter will focus on the clinical presentation, pathophysiology, and treatment of these increasingly recognized disorders.

The aim of the study was to investigate the effect of microbial immune enteral nutrition by microecopharmaceutics and deep sea fish oil and glutamine and Peptisorb on the patients with acute radiation enteritis in bowel function and immune status. From June 2010 to January 2013, 46 acute radiation enteritis patients in Liaocheng People’s Hospital were randomized into the microbial immune enteral nutrition group and the control group: 24 patients in treatment group and 22 patients in control group. The immune microbial nutrition was given to the study group, but not to the control group. The concentration of serum albumin and prealbumin and the number of CD 3 + T cell, CD 4 + T cell, CD 8 + T cell, CD 4 + /CD 8 + and natural killer cell of the two groups were detected on the 1, 7 and 14 days after treatment. The arm muscle circumference and triceps skinfold thickness (TSF) were recorded, and the tolerance of the two groups for enteral nutrition and intestinal symptoms was collected and then comparing the two indicators and get results. The tolerance of microbial immune enteral nutrition group about abdominal pain, bloating and diarrhea was better than the control group ( P values were 0.018, 0.04 and 0.008 after 7 days; P values were 0.018, 0.015 and 0.002 after 14 days); and the cellular immune parameters were better than the control group( △ P  = 0.008, ▲ P  = 0.039, ☆ P  = 0.032); No difference was found in nutrition indicators. To the patients with acute radiation enteritis, microbial immune enteral nutrition could improve the patient’s immune status, and the tolerance of enteral nutrition could be better for the bowel function and the patients’ rehabilitation.

BackgroundCurrent microbiome-based therapeutics face two prominent issues: the limited clinical efficacy of probiotics and the significant variability in the efficacy of microbiota transplantation across different diseases. Although washed microbiota transplantation (WMT) is a new faecal microbiota transplantation, a single therapeutic agent cannot be universally effective for multiple dysbiosis-related diseases.ObjectiveWe introduced a new therapeutic concept, X-augmented WMT (X-auWMT), which combines a disease-specific beneficial microbe, ‘X’, with WMT to enhance its effectiveness. Our goal was to identify a candidate ‘X’ bacterium to augment WMT efficacy and examine the efficacy of X-auWMT in animal models of radiation enteritis (RE).DesignWe conducted a prospective, non-randomised cohort study on a cohort of abdominal or pelvic cancer patients who developed RE after radiotherapy to identify a potential beneficial microbe. We used RE mouse models to evaluate the efficacy of X-auWMT compared with WMT. Multiomics analyses and experiments were undertaken to elucidate the underlying mechanisms.ResultsWMT significantly alleviated multiple clinical symptoms in RE patients compared with routine treatments. We identified Holdemanella biformis as a candidate ‘X’ bacterium within the RE cohort and developed Hb-auWMT. Hb-auWMT significantly mitigated radiation-induced injury compared with WMT, exhibiting enhanced anti-apoptotic effects, improved maintenance of epithelial hypoxia, increased Treg cell levels and elevated butyrate and valerate levels in the RE mouse model. PPAR-γ is an essential pathway for the therapeutic efficacy of Hb-auWMT.ConclusionsThis study overcomes the aforementioned recognised limitations with probiotics and microbiota transplantation and provides a new research paradigm in the concept of microbiome-based therapeutics.

Necrotic enteritis (NE) is a severe intestinal disease, which can change gut microbiota and result in a high cost for the poultry industry worldwide. However, little is known regarding how the gut microbiota of NE chicken ileum are changed by Bacillus licheniformis . This study was conducted to investigate how ileum microbiota structure was changed by B. licheniformis in broiler chickens challenged with Clostridium perfringens -induced NE through Illumina MiSeq sequencing. The broilers were randomly separated into four groups: the negative control group (NC), the positive control group (PC), the fishmeal and coccidia group (FC), and the PC group supplied with feed containing B. licheniformis (BL). Compared to the PC and FC, alpha diversity, beta diversity, and the bacterial taxa of the ileum microbiota were more similar in BL and NC. Some genera, which were related to the NE control, became insignificant in BL with NC, such as Lactobacillus , Lactococcus , Bacteroides , Ruminococcus and Helicobacter . The PICRUSt analysis revealed that a tumour suppressor gene, p53, which was negatively correlated with Helicobacter , was enriched in the BL group. Our findings showed that the ileum microbiota disorder caused by NE in chickens was normalized by dietary B. licheniformis supplementation.

Glutamine has been proposed as a preventive treatment for toxicity related to cancer therapies. The aim of this study was to test the efficacy of glutamine in the prevention of radiation enteritis. A randomized, double-blind, controlled trial was performed including 69 patients who were assigned to receive either glutamine (Gln, 30 g/d) or placebo while they were receiving abdominal radiotherapy. Patients were re-evaluated 1 y after completion of treatment. The presence of chronic enteritis was assessed using the Radiation Therapy Oncology Group scale. Nutritional status was evaluated using subjective global assessment, weight, and bioimpedance. Relative risk (RR) and its confidence interval (CI) were also calculated. The trial initially included 69 patients (34 Gln, 35 placebo), but 11 patients were lost during follow-up (4 Gln, 7 placebo; P = 0.296). Chronic enteritis was developed by 14 % of patients: Gln 16.7 % versus placebo 11.1% (RR = 1.33; 95 % CI, 0.35–5.03; P = 0.540). Most cases of enteritis were grade I (75 %), with no differences between groups. The stool frequency increased after radiotherapy in patients who received Gln (from 1 ± 1 to 2 ± 2 stools per day, P = 0.012), but remained unchanged with placebo (1 ± 1 stools per day, P = 0.858; difference between groups P = 0.004). There were no differences between the two groups in terms of weight, fat mass, or fat-free mass index, or between patients with enteritis and those without intestinal toxicity. Chronic enteritis is a relatively infrequent phenomenon, and Gln administration during radiotherapy does not exert a protective effect. •Glutamine has been proposed as a nutrient with potential protective effects against the toxicity induced either by chemoradiotherapy, but few trials have studied this effect.•The administration of oral glutamine during abdominal radiotherapy was related with the development of gastrointestinal symptoms.•One year after finishing radiotherapy, the patients who received glutamine referred significant changes in stool frequency and characteristics.•Glutamine was not related to better nutritional outcomes compared with placebo.

Background Environmental enteric dysfunction (EED) is an acquired enteropathy of the small intestine, characterized by enteric inflammation, villus blunting and decreased crypt-to-villus ratio. EED has been associated with poor outcomes, including chronic malnutrition (stunting), wasting and reduced vaccine efficacy among children living in low-resource settings. As a result, EED may be a valuable interventional target for programs aiming to reduce childhood morbidity in low and middle-income countries. Main text Several highly plausible mechanisms link the proposed pathophysiology underlying EED to adverse outcomes, but causal attribution of these pathways has proved challenging. We provide an overview of recent studies evaluating the causes and consequences of EED. These include studies of the role of subclinical enteric infection as a primary cause of EED, and efforts to understand how EED-associated systemic inflammation and malabsorption may result in long-term morbidity. Finally, we outline recently completed and upcoming clinical trials that test novel interventions to prevent or treat this highly prevalent condition. Conclusions Significant strides have been made in linking environmental exposure to enteric pathogens and toxins with EED, and in understanding the multifactorial mechanisms underlying this complex condition. Further insights may come from several ongoing and upcoming interventional studies trialing a variety of novel management strategies.