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Rare Co-occurrence of Eosinophilic Esophagitis and Type 2B von Willebrand Disease: Implications for Endoscopic Surveillance and Esophageal Dilation.

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Rare Co-occurrence of Eosinophilic Esophagitis and Type 2B von Willebrand Disease: Implications for Endoscopic Surveillance and Esophageal Dilation.

ACG Case Rep J. 2019 May;6(5):e00069

Authors: Corder SR, Weston BW, Dellon ES

Abstract
Eosinophilic esophagitis (EoE) and type 2B von Willebrand disease (vWD) are both rare diseases, and the co-occurrence is unlikely. Patients with EoE often need recurrent endoscopic dilations and esophageal biopsies, and the safety of these procedures in the setting of bleeding disorders is not well described in the literature. We describe successful management strategies in a patient with co-existing EoE and type 2B vWD who required multiple dilations and biopsies. This approach might be used for patients with other esophageal disorders and type 2B vWD as well.

PMID: 31616746 [PubMed]

Concordance between gene expression in peripheral whole blood and colonic tissue in children with inflammatory bowel disease.

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Concordance between gene expression in peripheral whole blood and colonic tissue in children with inflammatory bowel disease.

PLoS One. 2019;14(10):e0222952

Authors: Palmer NP, Silvester JA, Lee JJ, Beam AL, Fried I, Valtchinov VI, Rahimov F, Kong SW, Ghodoussipour S, Hood HC, Bousvaros A, Grand RJ, Kunkel LM, Kohane IS

Abstract
BACKGROUND: Presenting features of inflammatory bowel disease (IBD) are non-specific. We hypothesized that mRNA profiles could (1) identify genes and pathways involved in disease pathogenesis; (2) identify a molecular signature that differentiates IBD from other conditions; (3) provide insight into systemic and colon-specific dysregulation through study of the concordance of the gene expression.
METHODS: Children (8-18 years) were prospectively recruited at the time of diagnostic colonoscopy for possible IBD. We used transcriptome-wide mRNA profiling to study gene expression in colon biopsies and paired whole blood samples. Using blood mRNA measurements, we fit a regression model for disease state prediction that was validated in an independent test set of adult subjects (GSE3365).
RESULTS: Ninety-eight children were recruited [39 Crohn's disease, 18 ulcerative colitis, 2 IBDU, 39 non-IBD]. There were 1,118 significantly differentially (IBD vs non-IBD) expressed genes in colon tissue, and 880 in blood. The direction of relative change in expression was concordant for 106/112 genes differentially expressed in both tissue types. The regression model from the blood mRNA measurements distinguished IBD vs non-IBD disease status in the independent test set with 80% accuracy using only 6 genes. The overlap of 5 immune and metabolic pathways in the two tissue types was significant (p<0.001).
CONCLUSIONS: Blood and colon tissue from patients with IBD share a common transcriptional profile dominated by immune and metabolic pathways. Our results suggest that peripheral blood expression levels of as few as 6 genes (IL7R, UBB, TXNIP, S100A8, ALAS2, and SLC2A3) may distinguish patients with IBD from non-IBD.

PMID: 31618209 [PubMed - in process]

Consideration of Maternal Anti-enterocyte IgA Transfer With Resulting Infantile Alloimmune Enteropathy.

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Consideration of Maternal Anti-enterocyte IgA Transfer With Resulting Infantile Alloimmune Enteropathy.

ACG Case Rep J. 2019 Jun;6(6):e00093

Authors: Luginbill JB, Rutledge JC, Giefer MJ

Abstract
Autoimmune enteropathy is a rare cause of infantile diarrhea. Cases typically involve infants with a protracted course of diarrhea found to have underlying autoimmune disease or immune dysfunction, leading to chronic intestinal inflammation. We describe a case of immune-mediated enteropathy in an infant with no identifiable autoimmune disease. The patient was exclusively breastfed by his mother who had Crohn's disease, and he was found to have circulating anti-enterocyte immunoglobulin A (IgA) antibody. There was no circulating anti-enterocyte immunoglobulin G or immunoglobulin M. The patient's disease and symptoms resolved with cessation of breastfeeding, and no immunomodulatory medications have been needed in 20 months of follow-up. The case raises suspicion for alloimmune disease, and it is hypothesized that intestinal injury was mediated by maternally transmitted anti-enterocyte IgA antibody.

PMID: 31616766 [PubMed]

Optogenetic Activation of Colon Epithelium of the Mouse Produces High-Frequency Bursting in Extrinsic Colon Afferents and Engages Visceromotor Responses.

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Optogenetic Activation of Colon Epithelium of the Mouse Produces High-Frequency Bursting in Extrinsic Colon Afferents and Engages Visceromotor Responses.

J Neurosci. 2018 06 20;38(25):5788-5798

Authors: Makadia PA, Najjar SA, Saloman JL, Adelman P, Feng B, Margiotta JF, Albers KM, Davis BM

Abstract
Epithelial cells of the colon provide a vital interface between the internal environment (lumen of the colon) and colon parenchyma. To examine epithelial-neuronal signaling at this interface, we analyzed mice in which channelrhodopsin (ChR2) was targeted to either TRPV1-positive afferents or to villin-expressing colon epithelial cells. Expression of a ChR2-EYFP fusion protein was directed to either primary sensory neurons or to colon epithelial cells by crossing Ai32 mice with TRPV1-Cre or villin-Cre mice, respectively. An ex vivo preparation of the colon was used for single-fiber analysis of colon sensory afferents of the pelvic nerve. Afferents were characterized using previously described criteria as mucosal, muscular, muscular-mucosal, or serosal and then tested for blue light-induced activation. Light activation of colon epithelial cells produced robust firing of action potentials, similar to that elicited by physiologic stimulation (e.g., circumferential stretch), in 50.5% of colon afferents of mice homozygous for ChR2 expression. Light-induced activity could be reduced or abolished in most fibers using a cocktail of purinergic receptor blockers suggesting ATP release by the epithelium contributed to generation of sensory neuron action potentials. Using electromyographic recording of visceromotor responses we found that light stimulation of the colon epithelium evoked behavioral responses in Vil-ChR2 mice that was similar to that seen with balloon distension of the colon. These ex vivo and in vivo data indicate that light stimulation of colon epithelial cells alone, without added mechanical or chemical stimuli, can directly activate colon afferents and elicit behavioral responses.SIGNIFICANCE STATEMENT Abdominal pain that accompanies inflammatory diseases of the bowel is particularly vexing because it can occur without obvious changes in the structure or inflammatory condition of the colon. Pain reflects abnormal sensory neuron activity that may be controlled in part by release of substances from lining epithelial cells. In support of this mechanism we determined that blue-light stimulation of channelrhodopsin-expressing colon epithelial cells could evoke action potential firing in sensory neurons and produce changes in measures of behavioral sensitivity. Thus, activity of colon epithelial cells alone, without added mechanical or chemical stimuli, is sufficient to activate pain-sensing neurons.

PMID: 29789376 [PubMed - indexed for MEDLINE]

Management of inflammatory bowel disease in children: It is time for an individualised approach.

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Management of inflammatory bowel disease in children: It is time for an individualised approach.

J Paediatr Child Health. 2019 Oct 15;:

Authors: Grover Z, Alex G

Abstract
Paediatric-onset inflammatory bowel disease (PO-IBD) is associated with greater morbidity compared to adult-onset IBD. However, as not all children with PO-IBD will have poor outcome and the best management decisions involve weighing risks versus benefit and wishes of patient's and family, we review risk factors of IBD progression in children and summarise rapidly expanding treatment choices, potential drug-related adverse events and risk minimisation strategies, ending with new treatment paradigms focusing on long-term goal of intestinal healing. For the purpose of this article, we have outlined the conventional approach, including medications currently licenced and available for use in Australia for paediatric IBD through the Pharmaceutical Benefit Scheme and briefly discuss other promising therapies that are shown to be effective in adults but are undergoing paediatric clinical trials.

PMID: 31613039 [PubMed - as supplied by publisher]

Familial Celiac Disease Remission as a Result of a Full Donor Immunologic Recovery After Sibling Cord Blood Transplantation for Chronic Granulomatous Disease: A Case Report.

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Familial Celiac Disease Remission as a Result of a Full Donor Immunologic Recovery After Sibling Cord Blood Transplantation for Chronic Granulomatous Disease: A Case Report.

Transplant Proc. 2019 Oct 11;:

Authors: Janeczko-Czarnecka M, Kałwak K, Ussowicz M

Abstract
We present a case report of a boy diagnosed with both chronic granulomatous disease (CGD) and familial celiac disease (CD) who underwent cord blood transplantation from a partially matched sibling donor. The presentation of CD resembled Crohn-like enteropathy, which is a canonical manifestation of CGD. Nearly 1 year post-hematopoietic stem cell transplantation (HSCT), a gluten-containing diet was reintroduced, and no reappearance of clinical, serologic, or histologic markers of CD was observed. The relatively high incidence of rare genetic diseases in pediatric patients suggests the need for additional caution in the interpretation of symptoms mimicking already known hallmarks of more common conditions. In addition, the presented data confirm the previous rare observations that allogeneic HSCT leads to durable induction of gluten tolerance in patients with CD, which can warrant its use in patients with refractory subtypes of CD.

PMID: 31611125 [PubMed - as supplied by publisher]

IL-33 Induces Murine Intestinal Goblet Cell Differentiation Indirectly via Innate Lymphoid Cell IL-13 Secretion.

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IL-33 Induces Murine Intestinal Goblet Cell Differentiation Indirectly via Innate Lymphoid Cell IL-13 Secretion.

J Immunol. 2019 01 15;202(2):598-607

Authors: Waddell A, Vallance JE, Hummel A, Alenghat T, Rosen MJ

Abstract
Regulation of the intestinal mucus layer by goblet cells is important for preventing inflammation and controlling infection. IL-33, a cytokine upregulated in inflammatory bowel disease and helminth infection, induces intestinal goblet cells, but the mechanism remains unclear. Enteroids are three-dimensional structures of primary small intestinal epithelial cells that contain all differentiated intestinal epithelial cell types. We developed an enteroid-immune cell coculture model to determine the mechanism through which IL-33 affects intestinal goblet cell differentiation. We report that IL-33 does not directly induce goblet cell differentiation in murine enteroids; however, IL-13, a cytokine induced by IL-33, markedly induces goblet cells and gene expression consistent with goblet cell differentiation. When enteroids are cocultured with CD90+ mesenteric lymph node cells from IL-33-treated mice, IL-33 then induces IL-13 secretion by group 2 innate lymphoid cells and enteroid gene expression consistent with goblet cell differentiation. In cocultures, IL-33-induced Muc2 expression is dependent on enteroid Il4ra expression, demonstrating a requirement for IL-13 signaling in epithelial cells. In vivo, IL-33-induced intestinal goblet cell hyperplasia is dependent on IL-13. These studies demonstrate that IL-33 induces intestinal goblet cell differentiation not through direct action on epithelial cells but indirectly through IL-13 production by goup 2 innate lymphoid cells.

PMID: 30530480 [PubMed - indexed for MEDLINE]

The Treatment of Inflammatory Bowel Disease in Patients with Selected Primary Immunodeficiencies.

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The Treatment of Inflammatory Bowel Disease in Patients with Selected Primary Immunodeficiencies.

J Clin Immunol. 2018 07;38(5):579-588

Authors: Shouval DS, Kowalik M, Snapper SB

Abstract
The gastrointestinal tract is heavily populated with innate and adaptive immune cells that have an active role in preservation of mucosal homeostasis and prevention of inflammation. Inflammatory bowel diseases are thought to result from dysregulated immune function that is influenced by genetic background, environmental triggers, and microbiome changes. While most inflammatory bowel disease patients present in adolescent years or adulthood, in a minority of cases, the disease develops early in life, and in some of these young patients, a monogenic disease causing intestinal inflammation can be identified. Many of these conditions result from mutations in immune-mediated genes and can present with or without concomitant recurrent infections. In this review, we will discuss the treatment of patients with selected primary immunodeficiencies and inflammatory bowel diseases. We will focus on five conditions resulting from mutations in IL10/IL10 receptor, NADPH oxidase complex, XIAP, LRBA, and CTLA-4.

PMID: 29956079 [PubMed - indexed for MEDLINE]

Tissue transglutaminase autoantibodies in children with newly diagnosed type 1 diabetes are related to human leukocyte antigen but not to islet autoantibodies: A Swedish nationwide prospective population-based cohort study.

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Tissue transglutaminase autoantibodies in children with newly diagnosed type 1 diabetes are related to human leukocyte antigen but not to islet autoantibodies: A Swedish nationwide prospective population-based cohort study.

Autoimmunity. 2018 08;51(5):221-227

Authors: Cerqueiro Bybrant M, Grahnquist L, Örtqvist E, Andersson C, Forsander G, Elding Larsson H, Lernmark Å, Ludvigsson J, Marcus C, Carlsson A, Ivarsson SA

Abstract
OBJECTIVES: This study explored the association between tissue transglutaminase autoantibody (tTGA), high-risk human leucocyte antigen (HLA) genotypes and islet autoantibodies in children with newly diagnosed type 1 diabetes (T1D).
PATIENTS AND METHODS: Dried blood spots and serum samples were taken at diagnosis from children <18 years of age participating in Better Diabetes Diagnosis (BDD), a Swedish nationwide prospective cohort study of children newly diagnosed with T1D. We analyzed tTGA, high-risk HLA DQ2 and DQ8 (DQX is neither DQ2 nor DQ8) and islet auto-antibodies (GADA, IA-2A, IAA, and three variants of Zinc transporter; ZnT8W, ZnT8R, and ZnT8QA).
RESULTS: Out of 2705 children diagnosed with T1D, 85 (3.1%) had positive tTGA and 63 (2.3%) had borderline values. The prevalence of tTGA was higher in children with the HLA genotypes DQ2/2, DQ2/X or DQ2/8 compared to those with DQ8/8 or DQ8/X (p = .00001) and those with DQX/X (p ≤ .00001). No significant differences were found in relation to islet autoantibodies or age at diagnosis, but the presence of tTGA was more common in girls than in boys (p = .018).
CONCLUSION: tTGA at T1D diagnosis (both positive and borderline values 5.4%) was higher in girls and in children homozygous for DQ2/2, followed by children heterozygous for DQ2. Only children with DQ2 and/or DQ8 had tTGA. HLA typing at the diagnosis of T1D can help to identify those without risk for CD.

PMID: 30444426 [PubMed - indexed for MEDLINE]

Isolation of Lamina Propria Mononuclear Cells from Murine Colon Using Collagenase E.

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Isolation of Lamina Propria Mononuclear Cells from Murine Colon Using Collagenase E.

J Vis Exp. 2019 Sep 26;(151):

Authors: McManus D, Novaira HJ, Hamers AAJ, Pillai AB

Abstract
The intestine is the home to the largest number of immune cells in the body. The small and large intestinal immune systems police exposure to exogenous antigens and modulate responses to potent microbially derived immune stimuli. For this reason, the intestine is a major target site of immune dysregulation and inflammation in many diseases including but, not limited to inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, graft-versus-host disease (GVHD) after bone marrow transplantation (BMT), and many allergic and infectious conditions. Murine models of gastrointestinal inflammation and colitis are heavily used to study GI complications and to pre-clinically optimize strategies for prevention and treatment. Data gleaned from these models via isolation and phenotypic analysis of immune cells from the intestine is critical to further immune understanding that can be applied to ameliorate gastrointestinal and systemic inflammatory disorders. This report describes a highly effective protocol for the isolation of mononuclear cells (MNC) from the colon using a mixed silica-based density gradient interface. This method reproducibly isolates a significant number of viable leukocytes while minimizing contaminating debris, allowing subsequent immune phenotyping by flow cytometry or other methods.

PMID: 31609324 [PubMed - in process]

Infliximab for pediatric patients with ulcerative colitis: a phase 3, open-label, uncontrolled, multicenter trial in Japan.

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Infliximab for pediatric patients with ulcerative colitis: a phase 3, open-label, uncontrolled, multicenter trial in Japan.

BMC Pediatr. 2019 Oct 13;19(1):351

Authors: Tajiri H, Arai K, Kagimoto S, Kunisaki R, Hida N, Sato N, Yamada H, Nagano M, Susuta Y, Ozaki K, Kondo K, Hibi T

Abstract
BACKGROUND: Pediatric ulcerative colitis (UC) is typically more extensive and has a more active disease course than adult UC, and requires early treatment augmentation to achieve and maintain disease remission. The present study aimed to investigate the efficacy, safety, and pharmacokinetic profile of infliximab (IFX) in pediatric patients with moderate-to-severe UC and inadequate response to existing treatment.
METHODS: This open-label, uncontrolled, multicenter, Phase 3 trial was conducted at 17 centers in Japan between April 2012 and September 2014. Pediatric patients (aged 6-17 years) diagnosed with moderate-to-severe UC received a treatment protocol comprising 5 mg/kg IFX at Weeks 0, 2, and 6, and Clinical Activity Index (CAI)-based responders at Week 8 also received treatment at 8-week intervals at Weeks 14 and 22, with a final evaluation at Week 30.
RESULTS: A total of 21 patients were treated in this study. IFX therapy rapidly improved clinical symptoms, and this effect was maintained for up to 30 weeks. Overall CAI-based remission rate was 42.9% and overall Pediatric Ulcerative Colitis Activity Index (PUCAI)-based remission rate was 19.0%. Median partial Mayo score was 6.0 at baseline and 4.0 at Week 30 (overall). Among the eight patients who underwent sigmoidoscopy, Mayo response was achieved at Week 30 (overall) in three patients (37.5%). Trough serum IFX concentrations in Week 8 CAI-based responders were maintained throughout the study period. Adverse events and serious adverse events were observed in 95.2 and 14.3% of patients, respectively.
CONCLUSIONS: These results support the use of IFX in the treatment of pediatric patients with UC with inadequate response to existing treatment.
TRIAL REGISTRATION: ClinicalTrials.gov, registration number: NCT01585155 .

PMID: 31607268 [PubMed - in process]

The Role of Dietary Nutrients in Inflammatory Bowel Disease.

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The Role of Dietary Nutrients in Inflammatory Bowel Disease.

Front Immunol. 2018;9:3183

Authors: Sugihara K, Morhardt TL, Kamada N

Abstract
Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD remains incompletely understood, accumulating evidence suggests that various environmental factors, including dietary nutrients, contribute to its pathogenesis. Dietary nutrients are known to have an impact on host physiology and diseases. The interactions between dietary nutrients and intestinal immunity are complex. Dietary nutrients directly regulate the immuno-modulatory function of gut-resident immune cells. Likewise, dietary nutrients shape the composition of the gut microbiota. Therefore, a well-balanced diet is crucial for good health. In contrast, the relationships among dietary nutrients, host immunity and/or the gut microbiota may be perturbed in the context of IBD. Genetic predispositions and gut dysbiosis may affect the utilization of dietary nutrients. Moreover, the metabolism of nutrients in host cells and the gut microbiota may be altered by intestinal inflammation, thereby increasing or decreasing the demand for certain nutrients necessary for the maintenance of immune and microbial homeostasis. Herein, we review the current knowledge of the role dietary nutrients play in the development and the treatment of IBD, focusing on the interplay among dietary nutrients, the gut microbiota and host immune cells. We also discuss alterations in the nutritional metabolism of the gut microbiota and host cells in IBD that can influence the outcome of nutritional intervention. A better understanding of the diet-host-microbiota interactions may lead to new therapeutic approaches for the treatment of IBD.

PMID: 30697218 [PubMed - indexed for MEDLINE]

Non-Celiac Gluten Sensitivity in patients with severe abdominal pain and bloating: The accuracy of ALCAT 5.

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Non-Celiac Gluten Sensitivity in patients with severe abdominal pain and bloating: The accuracy of ALCAT 5.

Clin Nutr ESPEN. 2018 12;28:127-131

Authors: Di Stefano M, Pesatori EV, Manfredi GF, De Amici M, Grandi G, Gabriele A, Iozzi D, Di Fede G

Abstract
BACKGROUND AND AIMS: Non-Celiac Gluten Sensitivity (NCGS) is a recently proposed clinical condition causing both intestinal and extra-intestinal symptoms, without gastrointestinal lesions, which improve on avoiding gluten intake, in the absence of celiac disease and wheat allergy. The prevalence of this condition is still a matter of debate, in part due to the very recent introduction of an accepted diagnostic test, a double-blind, placebo controlled gluten challenge. However, this is a lengthy and cumbersome procedure, theoretically burdened by a significant reduction of patient compliance. ALCAT 5 is an automated in vitro test evaluating the toxic effect of gluten on neutrophils by the exposure of these cells to a gluten-containing extract of gluten-containing cereals. The test is very simple to perform, the results are rapidly obtained, and might represent, if sufficiently accurate, a promising alternative to diagnose gluten intolerance. The aim of this study was the comparison of ALCAT 5 results with those of a double-blind, placebo-controlled, gluten challenge, in a group of patients with clinically-suspected NCGS.
METHODS: Twenty-five patients (M/F 3/22, mean age 32 ± 4 yrs) with severe functional abdominal pain and bloating, who had previously undergone the ALCAT 5 test, were enrolled. All the subjects reported their symptoms on a gluten-containing diet and considered gluten the causal agent. Following the Salerno Experts' Criteria, they underwent a double-blind, placebo controlled trial with gluten vs placebo. A mean value during gluten ingestion >30% of the value during placebo was considered as indicative of gluten sensitivity.
RESULTS: After blinded administration of gluten, 13 out of 25 (52%) patients showed an increase in the severity of abdominal pain, and 11 out of 25 (44%) showed an increase in the severity of abdominal bloating. Considering these two symptoms together, in 16 patients out of 25 (64%), blinded gluten administration induced an increase of abdominal pain and/or bloating. The ALCAT 5 test proved to be positive in 20 and negative in 5 patients. In sixteen patients out of 25 the result of ALCAT 5 agreed with the double-blind trial (64%). In particular, both tests were positive in 14 patients and negative in 2.
CONCLUSIONS: In this subgroup of patients, ALCAT 5 could be used to support the clinical suspicion of the presence of NCGS and to address these patients to a blinded gluten challenge.

PMID: 30390869 [PubMed - indexed for MEDLINE]

Associations between the severity of reflux esophagitis in children and changes in oxidative stress, serum inflammation, vasoactive intestinal peptide and motilin.

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Associations between the severity of reflux esophagitis in children and changes in oxidative stress, serum inflammation, vasoactive intestinal peptide and motilin.

Exp Ther Med. 2019 Nov;18(5):3509-3513

Authors: Deng Y, Pan L, Qian W

Abstract
Changes in the levels of serum oxidative stress indexes, gastrointestinal hormones and inflammatory factors in children with different severity of reflux esophagitis (RE) were detected. Sixty child patients diagnosed with gastroesophageal reflux disease (GERD) via gastroscopy were selected and divided into non-erosive reflux disease group (NERD group, n=12) and RE group (n=48) according to whether there was esophageal mucosal injury. In RE group, the patients were further divided into grade I RE group (n=15), grade II RE group (n=18) and grade III RE group (n=15) based on the severity of mucosal injury. None of the child patients took PPI and domperidone within 2 weeks before enrollment. The content of malondialdehyde (MDA) and total superoxide dismutase (T-SOD) in the esophageal mucosa was detected. The changes in the levels of serum vasoactive intestinal peptide (VIP), motilin, interleukin-1β (IL-1β), IL-8 and tumor necrosis factor-α (TNF-α) were determined. The DeMeester score was the highest in grade III RE group, followed by grade II RE group, grade I RE group and NERD group (P<0.05). The content of MDA in the esophageal mucosa was higher in RE group than that in NERD group, and the T-SOD activity declined with the increased severity of injury (P<0.05). In the three RE groups, the level of plasma VIP was significantly higher, while the motilin level was remarkably lower than those in NERD group (P<0.05). With the increased severity of disease, the expression levels of serum IL-1β, IL-8 and TNF-α in RE group were gradually raised (P<0.05). RE patients have strong oxidative stress and inflammatory response, an increased level of serum VIP, a regulator of gastrointestinal motility, and a decreased level of motilin. Controlling the changes in the above factors using effective treatment means can improve the development of GERD.

PMID: 31602227 [PubMed]

Vascular Changes in Eosinophilic Esophagitis (EOE), Report of an Unusual Case.

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Vascular Changes in Eosinophilic Esophagitis (EOE), Report of an Unusual Case.

Fetal Pediatr Pathol. 2019 Oct 11;:1-6

Authors: Mahjoub FE, Fallahi GH, Niknejad N

Abstract
Background: Submucosal or lamina propria arteries are not often included in esophageal biopsies. We report an esophageal biopsy with eosinophilic esophagitis (EOE) overlying small arteries with medial hypertrophy to the point of obstruction. Case presentation: A two-year-old boy with a 1-year history of asthma frequently vomited after coughing. Esophageal biopsy showed EOE. Within the lamina propria there were small arteries with markedly thickened media to the point of luminal obstruction next to a hyperplastic lymphoid aggregate. There was no significant inflammatory infiltrate in the arterial walls. Subsequent biopsies did not show these vascular changes. Conclusion: Small artery changes in EOE have not previously been reported, and although the significance is unknown, in this case may be incidental to eosinophilic esophagitis.

PMID: 31603366 [PubMed - as supplied by publisher]

Migratory DCs activate TGF-β to precondition naïve CD8+ T cells for tissue-resident memory fate.

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Migratory DCs activate TGF-β to precondition naïve CD8+ T cells for tissue-resident memory fate.

Science. 2019 10 11;366(6462):

Authors: Mani V, Bromley SK, Äijö T, Mora-Buch R, Carrizosa E, Warner RD, Hamze M, Sen DR, Chasse AY, Lorant A, Griffith JW, Rahimi RA, McEntee CP, Jeffrey KL, Marangoni F, Travis MA, Lacy-Hulbert A, Luster AD, Mempel TR

Abstract
Epithelial resident memory T (eTRM) cells serve as sentinels in barrier tissues to guard against previously encountered pathogens. How eTRM cells are generated has important implications for efforts to elicit their formation through vaccination or prevent it in autoimmune disease. Here, we show that during immune homeostasis, the cytokine transforming growth factor β (TGF-β) epigenetically conditions resting naïve CD8+ T cells and prepares them for the formation of eTRM cells in a mouse model of skin vaccination. Naïve T cell conditioning occurs in lymph nodes (LNs), but not in the spleen, through major histocompatibility complex class I-dependent interactions with peripheral tissue-derived migratory dendritic cells (DCs) and depends on DC expression of TGF-β-activating αV integrins. Thus, the preimmune T cell repertoire is actively conditioned for a specialized memory differentiation fate through signals restricted to LNs.

PMID: 31601741 [PubMed - in process]

Reply.

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Reply.

Gastroenterology. 2019 10;157(4):1161-1162

Authors: Gerasimidis K, Svolos V, Nichols B, Papadopoulou R, Quince C, Ijaz UZ, Milling S, Gaya DR, Russell RK, Hansen R

PMID: 31408620 [PubMed - indexed for MEDLINE]

Gut microbiota composition and functional changes in inflammatory bowel disease and irritable bowel syndrome.

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Gut microbiota composition and functional changes in inflammatory bowel disease and irritable bowel syndrome.

Sci Transl Med. 2018 12 19;10(472):

Authors: Vich Vila A, Imhann F, Collij V, Jankipersadsing SA, Gurry T, Mujagic Z, Kurilshikov A, Bonder MJ, Jiang X, Tigchelaar EF, Dekens J, Peters V, Voskuil MD, Visschedijk MC, van Dullemen HM, Keszthelyi D, Swertz MA, Franke L, Alberts R, Festen EAM, Dijkstra G, Masclee AAM, Hofker MH, Xavier RJ, Alm EJ, Fu J, Wijmenga C, Jonkers DMAE, Zhernakova A, Weersma RK

Abstract
Changes in the gut microbiota have been associated with two of the most common gastrointestinal diseases, inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Here, we performed a case-control analysis using shotgun metagenomic sequencing of stool samples from 1792 individuals with IBD and IBS compared with control individuals in the general population. Despite substantial overlap between the gut microbiome of patients with IBD and IBS compared with control individuals, we were able to use gut microbiota composition differences to distinguish patients with IBD from those with IBS. By combining species-level profiles and strain-level profiles with bacterial growth rates, metabolic functions, antibiotic resistance, and virulence factor analyses, we identified key bacterial species that may be involved in two common gastrointestinal diseases.

PMID: 30567928 [PubMed - indexed for MEDLINE]

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