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Effect of elemental diet on mucosal immunopathology and clinical symptoms in type 1 refractory celiac disease.

https://arctichealth.org/en/permalink/ahliterature83166
Source
Clin Gastroenterol Hepatol. 2005 Sep;3(9):875-85
Publication Type
Article
Date
Sep-2005
Author
Olaussen Richard Willfred
Løvik Astrid
Tollefsen Stig
Andresen Per Arne
Vatn Morten H
De Lange Thomas
Bratlie Jorunn
Brandtzaeg Per
Farstad Inger Nina
Lundin Knut E A
Author Affiliation
Laboratory for Immunohistochemistry and Immunopathology, Institute of Pathology, University of Oslo, Oslo, Norway.
Source
Clin Gastroenterol Hepatol. 2005 Sep;3(9):875-85
Date
Sep-2005
Language
English
Publication Type
Article
Keywords
Adult
Aged
Antigens, CD3 - metabolism
Biopsy
Body mass index
CD8-Positive T-Lymphocytes - metabolism
Celiac Disease - diet therapy - immunology - metabolism - pathology
Diet, Protein-Restricted
Duodenum - immunology - pathology
Female
Flow Cytometry
Food, Formulated
Humans
Immunohistochemistry
Immunophenotyping
Interferon Type II - metabolism
Interleukin-15 - metabolism
Intestinal Mucosa - immunology - metabolism - pathology
Male
Middle Aged
Norway
RNA, Messenger - metabolism
Receptors, Antigen, T-Cell - metabolism
T-Lymphocytes - metabolism
Treatment Outcome
Abstract
BACKGROUND & AIMS: Patients with celiac disease (CD) who do not improve or exhibit villous atrophy on a gluten-free diet may have type 1 refractory CD (RCD) with a polyclonal mucosal T-cell infiltrate, or type 2 RCD with a monoclonal infiltrate, also termed cryptic T-cell lymphoma. Both conditions are difficult to treat. Here we describe the effects of a nonimmunogenic elemental diet on clinical symptoms and mucosal immunopathology in type 1 RCD. METHODS: Ten CD patients on a strict gluten-free diet were diagnosed with type 1 RCD after extensive clinical evaluation in a tertiary referral hospital. A 4-week amino-acid-based liquid elemental diet regimen was given with no other treatment, except in 1 patient who also received methotrexate. Duodenal biopsy specimens were obtained before and after treatment for histologic assessment, immunophenotyping of intraepithelial lymphocytes, T-cell receptor clonality, mucosal interleukin (IL)-15 expression, flow-cytometric analysis of interferon (IFN)-gamma-secreting T cells, and whole biopsy specimen IFN-gamma messenger RNA determination. RESULTS: Nine patients completed the treatment; however, 1 patient did not tolerate the diet. Histologic improvement and reduced epithelial IL-15 were seen in 8 patients, whereas IFN-gamma-secreting mucosal T cells and IFN-gamma messenger RNA levels decreased in 4 and 7 patients, respectively. Clinical improvement was noted in 6 patients, with 1 patient showing normalization of hypoalbuminemia. Three patients could discontinue their total parenteral nutrition. CONCLUSIONS: Persistent mucosal IFN-gamma and IL-15 production often occurs in type 1 RCD despite conventional treatment. Elemental diet is a therapeutic option that can provide long-term immunopathologic and clinical improvement of this difficult condition.
PubMed ID
16234025 View in PubMed
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Enhanced local immune response in children with prolonged gastrointestinal symptoms.

https://arctichealth.org/en/permalink/ahliterature29760
Source
Acta Paediatr. 2004 Dec;93(12):1601-7
Publication Type
Article
Date
Dec-2004
Author
J. Kokkonen
K. Holm
T J Karttunen
M. Mäki
Author Affiliation
Department of Paediatrics, University of Oulu, Oulu, Finland. jorma.kokkonen@ppshp.fi
Source
Acta Paediatr. 2004 Dec;93(12):1601-7
Date
Dec-2004
Language
English
Publication Type
Article
Keywords
Antigens, CD3 - immunology - metabolism
Atrophy - pathology
Celiac Disease - immunology - metabolism - pathology
Child
Duodenoscopy - methods
Duodenum - immunology - metabolism - pathology
Female
Food Hypersensitivity - diet therapy - immunology - metabolism
Gastroscopy - methods
HLA-DR Antigens
Humans
Immunohistochemistry
Intestinal Mucosa - immunology - metabolism
Lymphocyte Count
Male
Receptors, Antigen, T-Cell, alpha-beta - immunology - metabolism
Receptors, Antigen, T-Cell, gamma-delta - immunology - metabolism
T-Lymphocyte Subsets - immunology - metabolism
Abstract
AIM: Recently, we reported typical endoscopic findings and an increment in gammadelta+ T cells in the foregut among children with food-sensitive enteropathy other than coeliac disease. To find out the extend to which the upregulation of the local immune response might explain gastrointestinal (GI) complaints of the foregut, we sought to examine by the increment in gammadelta+ T cells a I-y consecutive series of children referred for recurrent GI complaints to a tertiary-level hospital. METHODS: A 1-y cohort of 102 children scheduled for gastroduodenoscopy were examined for mucosal histology and the densities of CD3+, alphabeta+ and alphabeta+ T-cell subsets from mid-duodenal specimens. The final diagnostic categories were used in analysing the data. RESULTS: Fifteen subjects showed villous atrophy and a high gammadelta+ T-cell density; the finding being compatible with coeliac disease (CD). At the other extreme, 20 subjects in whom diagnostic GI diseases were ruled out showed low densities and served as controls. The subjects reporting GI symptoms after an open food challenge with milk and/or cereals (n = 18) as well as children remitting with a milk- or cereal-eliminating diet but not responding to a challenge (n = 23) also expressed significantly higher densities of gammadelta+ T cells than the controls. In all, 45 of 102 children could be considered to have an elevated gamma6+ T-cell density as an indication of locally activated immune response. Lack of villous architecture and lymphonodular hyperplasia of the duodenal bulb as an endoscopic finding and atopic dermatitis but not the presence of DQ2 alleles showed a close association with these increased densities. CONCLUSION: Considering that an elevated incidence of gammadelta+ T cells is an indication of mucosal response against luminal antigens, up to half the children with prolonged GI symptoms have immune mediated disorder; CD and food allergy being the most obvious clinical entities.
PubMed ID
15841768 View in PubMed
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Heat shock protein expression is low in intestinal mucosa in juvenile idiopathic arthritis: a defect in immunoregulation?

https://arctichealth.org/en/permalink/ahliterature98119
Source
Scand J Rheumatol. 2010 May;39(3):212-8
Publication Type
Article
Date
May-2010
Author
M. Arvonen
M. Tikanmäki
P. Vähäsalo
T J Karttunen
Author Affiliation
Department of Paediatrics, University of Oulu, and Oulu University Hospital, Oulu, Finland.
Source
Scand J Rheumatol. 2010 May;39(3):212-8
Date
May-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Arthritis, Juvenile Rheumatoid - immunology - metabolism
Chaperonin 60 - immunology - metabolism
Child
Child, Preschool
DNA-Binding Proteins - immunology - metabolism
Duodenum - immunology - metabolism
Female
HSP70 Heat-Shock Proteins - immunology - metabolism
Histocompatibility Antigens Class I - immunology - metabolism
Humans
Ileum - immunology - metabolism
Immunohistochemistry
Inflammation - immunology - metabolism
Intestinal Mucosa - immunology - metabolism
Male
Statistics, nonparametric
T-Lymphocytes - immunology - metabolism
Transcription Factors - immunology - metabolism
Abstract
OBJECTIVES: Heat shock proteins (HSPs) are involved in the regulation of inflammation and in the maintenance of mucosal integrity. Their altered expression may be a marker of mucosal inflammation and also contribute to tissue injury. The small intestinal mucosa in children with juvenile idiopathic arthritis (JIA) shows signs of intestinal immune activation, such as increased intraepithelial cytotoxic lymphocyte counts. To further evaluate the characteristics of this immune activation in JIA, we have studied the expression of several HSPs, major histocompatibility complex (MHC) class I-related chain A (MICA), and the heat shock transcription factor 1 (HSF1) in intestinal biopsies from children with JIA. METHODS: We studied 15 patients with JIA. Controls included 13 children without JIA, studied for various gastrointestinal (GI) symptoms, but eventually shown not to have any GI disease. The subjects were examined by endoscopy. The expression of HSP60, HSP70, MICA, and HSF1 was analysed in ileal and duodenal biopsies by using immunohistochemistry. RESULTS: The expression levels of HSP60, MICA, and HSF1 were significantly lower in the duodenal epithelium in the JIA patients compared to the controls. MICA and HSF1 also showed lower expression in the ileal epithelium. The expression of HSP70 did not differ between the groups. CONCLUSIONS: The downregulation of HSP60, MICA, and HSF1 in small intestinal mucosa may indicate that intestinal epithelial cells show immune aberration in JIA. We speculate that the low heat shock response may play a role in the pathogenesis of JIA, interfering with mucosal integrity and local intestinal immunoregulation.
PubMed ID
20141486 View in PubMed
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Preterm Birth Reduces Nutrient Absorption With Limited Effect on Immune Gene Expression and Gut Colonization in Pigs.

https://arctichealth.org/en/permalink/ahliterature274297
Source
J Pediatr Gastroenterol Nutr. 2015 Oct;61(4):481-90
Publication Type
Article
Date
Oct-2015
Author
Mette V Østergaard
Malene S Cilieborg
Kerstin Skovgaard
Mette Schmidt
Per T Sangild
Stine B Bering
Source
J Pediatr Gastroenterol Nutr. 2015 Oct;61(4):481-90
Date
Oct-2015
Language
English
Publication Type
Article
Keywords
Animals
Biomarkers - metabolism
Cattle
Colostrum - immunology - metabolism
Crosses, Genetic
Denmark
Digestion
Disease Models, Animal
Dysbiosis - etiology - prevention & control
Enteritis - etiology - prevention & control
Enterocolitis, Necrotizing - etiology - prevention & control
Gastrointestinal Microbiome - immunology
Gene Expression Regulation, Developmental
Immunity, Innate
Immunity, Mucosal
Intestinal Absorption
Intestinal Mucosa - immunology - metabolism - microbiology - pathology
Jejunum - immunology - metabolism - microbiology - pathology
Malabsorption Syndromes - etiology - prevention & control
Premature Birth - metabolism - microbiology - pathology - physiopathology
Sus scrofa
Tissue Culture Techniques
Abstract
The primary risk factors for necrotizing enterocolitis (NEC) are preterm birth, enteral feeding, and gut colonization. It is unclear whether feeding and colonization induce excessive expression of immune genes that lead to NEC. Using a pig model, we hypothesized that reduced gestational age would upregulate immune-related genes and cause bacterial imbalance after birth.
Preterm (85%-92% gestation, n?=?53) and near-term (95%-99% gestation, n?=?69) pigs were delivered by cesarean section and euthanized at birth or after 2 days of infant formula or bovine colostrum feeding.
At birth, preterm delivery reduced 5 of 30 intestinal genes related to nutrient absorption and innate immunity, relative to near-term pigs, whereas 2 genes were upregulated. Preterm birth also reduced ex vivo intestinal glucose and leucine uptake (40%-50%), but failed to increase cytokine secretions from intestinal explants relative to near-term birth. After 2 days of formula feeding, NEC incidence was increased in preterm versus near-term pigs (47% vs 0%-13%). A total of 6 of the 30 genes related to immunity (TLR2, IL1B, and IL8), permeability (CLDN3, and OCLN), and absorption (SGLT) decreased in preterm pigs without affecting Gram-negative bacteria-related responses (TLR4, IKBA, NFkB1, TNFAIP3, and PAFA). Bacterial abundance tended to be higher in preterm versus near-term pigs (P?=?0.09), whereas the composition was unaffected.
Preterm birth predisposes to NEC and reduces nutrient absorption but does not induce upregulation of immune-related genes or cause bacterial dyscolonization in the neonatal period. Excessive inflammation and bacterial overgrowth may occur relatively late in NEC progression in preterm neonates.
PubMed ID
25883061 View in PubMed
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