Search results for " intestine"

showing 10 items of 132 documents

2020

α-Linolenic acid (ALA) is well-known for its anti-inflammatory activity. In contrast, the influence of an ALA-rich diet on intestinal microbiota composition and its impact on small intestine morphology are not fully understood. In the current study, we kept adult C57BL/6J mice for 4 weeks on an ALA-rich or control diet. Characterization of the microbial composition of the small intestine revealed that the ALA diet was associated with an enrichment in Prevotella and Parabacteroides. In contrast, taxa belonging to the Firmicutes phylum, including Lactobacillus, Clostridium cluster XIVa, Lachnospiraceae and Streptococcus, had significantly lower abundance compared to control diet. Metagenome p…

0301 basic medicine030109 nutrition & dieteticsNutrition and DieteticsbiologyFirmicutesChemistryStreptococcusLachnospiraceaebiology.organism_classificationmedicine.disease_causeMolecular biologySmall intestine03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structureLactobacillusPaneth cellmedicinePrevotellaArachidonic acidFood ScienceNutrients
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Subclinical gut inflammation in ankylosing spondylitis

2015

Purpose of review Subclinical gut inflammation has been described in a significant proportion of patients with ankylosing spondylitis (AS), up to 10% of them developing it during the time of clinically overt inflammatory bowel disease. Histologic, immunologic, and intestinal microbiota alterations characterize the AS gut. Recent findings Microbial dysbiosis as well as alterations of innate immune responses have been demonstrated in the gut of AS. Furthermore, a growing body of evidence suggests that the gut of AS patients may be actively involved in the pathogenesis of AS through the production of proinflammatory cytokines, such as IL-23p19, and the differentiation of potentially pathogenic…

0301 basic medicineAnkylosing spondylitis; Gut inflammation; Innate lymphoid cells; Interleukin-17; Interleukin-23; Adaptive Immunity; Animals; Cytokines; Disease Models Animal; Dysbiosis; Gastrointestinal Microbiome; Humans; Immunity Innate; Inflammation; Inflammatory Bowel Diseases; Intestines; Macrophages; Mice; Spondylitis Ankylosing; Rheumatology; Medicine (all)MacrophageAdaptive ImmunityInterleukin-23Inflammatory bowel diseaseGastroenterologyMiceInterleukin 23InnateMedicineSubclinical infectionMedicine (all)Interleukin-17digestive oral and skin physiologyInnate lymphoid cellIntestineIntestinesCytokinesmedicine.symptomHumanAnkylosingmedicine.medical_specialtyDisease ModelInflammationdigestive system03 medical and health sciencesRheumatologyInternal medicineInnate lymphoid cellAnimalsHumansSpondylitis AnkylosingCytokineSpondylitisGut inflammationSpondylitiInflammationAnkylosing spondylitisAnimalbusiness.industryMacrophagesInflammatory Bowel DiseaseImmunityInflammatory Bowel Diseasesmedicine.diseaseImmunity InnateDysbiosiGastrointestinal MicrobiomeAnkylosing spondylitiDisease Models Animal030104 developmental biologyDysbiosisbusinessDysbiosisCurrent Opinion in Rheumatology
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Deregulated Lipid Sensing by Intestinal CD36 in Diet-Induced Hyperinsulinemic Obese Mouse Model

2016

International audience; The metabolic syndrome (MetS) greatly increases risk of cardiovascular disease and diabetes and is generally associated with abnormally elevated postprandial triglyceride levels. We evaluated intestinal synthesis of triglyceride-rich lipoproteins (TRL) in a mouse model of the MetS obtained by feeding a palm oil-rich high fat diet (HFD). By contrast to control mice, MetS mice secreted two populations of TRL. If the smaller size population represented 44% of total particles in the beginning of intestinal lipid absorption in MetS mice, it accounted for only 17% after 4 h due to the secretion of larger size TRL. The MetS mice displayed accentuated postprandial hypertrigl…

0301 basic medicineCD36 Antigens[SDV]Life Sciences [q-bio]lcsh:Medicine030204 cardiovascular system & hematologyLipoprotein MetabolismMice0302 clinical medicineIntestinal mucosaHyperinsulinemiaIntestinal Mucosalcsh:ScienceMetabolic Syndromeeducation.field_of_studyMultidisciplinaryIntestinal lipid absorption3. Good healthPostprandialChain Fatty-Acidslipids (amino acids peptides and proteins)Research ArticleNonfasting Triglyceridesmedicine.medical_specialtyPopulationTransportDistal IntestineBiologyDiet High-FatAbsorption03 medical and health sciencesInsulin resistanceInternal medicineHyperinsulinismmedicineAnimalsCholesterol UptakeObesityeducationSecretion[ SDV ] Life Sciences [q-bio]Insulin-Resistancelcsh:RHypertriglyceridemiaLipid metabolismmedicine.diseaseLipid MetabolismDisease Models Animal030104 developmental biologyEndocrinologyGene Expression Regulationlcsh:Q[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Eosinophil depletion suppresses radiation-induced small intestinal fibrosis.

2017

Radiation-induced intestinal fibrosis (RIF) is a serious complication after abdominal radiotherapy for pelvic tumor or peritoneal metastasis. Herein, we show that RIF is mediated by eosinophil interactions with α-smooth muscle actin-positive (α-SMA+) stromal cells. Abdominal irradiation caused RIF especially in the submucosa (SM) of the small intestine, which was associated with the excessive accumulation of eosinophils in both human and mouse. Eosinophil-deficient mice showed markedly ameliorated RIF, suggesting the importance of eosinophils. After abdominal irradiation, chronic crypt cell death caused elevation of extracellular adenosine triphosphate, which in turn activated expression of…

0301 basic medicineChemokineStromal cellCCR303 medical and health sciencesChemokine receptorMiceIntestine SmallmedicineAnimalsIntestinal MucosaReceptorCCL11biologyChemistryGeneral Medicinerespiratory systemEosinophilFibrosisSmall intestineEosinophilsDisease Models AnimalRadiation Injuries Experimental030104 developmental biologymedicine.anatomical_structurebiology.proteinCancer researchScience translational medicine
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Specific norovirus interaction with Lewis x and Lewis a on human intestinal inflammatory mucosa during refractory inflammatory bowel disease

2021

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are progressive diseases affecting millions of people each year. Flare-ups during IBD result in severe mucosal alterations of the small intestine (in CD) and in the colon and rectum (in CD and UC).

0301 basic medicineCrohn’s diseaseMaleSeverity of Illness IndexInflammatory bowel diseasechemistry.chemical_compound0302 clinical medicineMedicineIntestinal MucosaCrohn's disease0303 health sciencesMiddle AgedImmunohistochemistryUlcerative colitisQR1-502HBGA3. Good healthmedicine.anatomical_structure030220 oncology & carcinogenesisImmunohistochemistry030211 gastroenterology & hepatologyFemalegut inflammationResearch ArticleAdultCA-19-9 Antigenmedicine.drug_classLewis X AntigenRectumMonoclonal antibodyMicrobiologydigestive systemVirusHost-Microbe BiologyYoung Adult03 medical and health sciencesAntigenHumansMolecular Biologyulcerative colitis030304 developmental biologybusiness.industryNorovirus[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologySialyl-Lewis AInflammatory Bowel Diseasesmedicine.diseasedigestive system diseasesSmall intestineGastrointestinal Tract030104 developmental biologySialyl-Lewis XchemistryinflammationImmunologybusiness[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Duodenal Bacteria From Patients With Celiac Disease and Healthy Subjects Distinctly Affect Gluten Breakdown and Immunogenicity

2016

Background & Aims Partially degraded gluten peptides from cereals trigger celiac disease (CD), an autoimmune enteropathy occurring in genetically susceptible persons. Susceptibility genes are necessary but not sufficient to induce CD, and additional environmental factors related to unfavorable alterations in the microbiota have been proposed. We investigated gluten metabolism by opportunistic pathogens and commensal duodenal bacteria and characterized the capacity of the produced peptides to activate gluten-specific T-cells from CD patients. Methods We colonized germ-free C57BL/6 mice with bacteria isolated from the small intestine of CD patients or healthy controls, selected for their in v…

0301 basic medicineGlutensDuodenumTissue transglutaminaseT-Lymphocytesdigestive systemMicrobiologyMice03 medical and health sciencesLactobacillusmedicineAnimalsHumansImmunogenetic Phenomenachemistry.chemical_classificationHepatologybiologyImmunogenicityGastroenterologynutritional and metabolic diseasesmedicine.diseasebiology.organism_classificationGlutendigestive system diseasesSmall intestineAltered Schaedler floraMice Inbred C57BLCeliac DiseaseLactobacillus030104 developmental biologymedicine.anatomical_structurechemistryBacterial TranslocationCase-Control StudiesPseudomonas aeruginosaImmunologybiology.proteinGliadinDysbiosisGastroenterology
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Lactobacilli Degrade Wheat Amylase Trypsin Inhibitors to Reduce Intestinal Dysfunction Induced by Immunogenic Wheat Proteins.

2019

Background & Aims Wheat-related disorders, a spectrum of conditions induced by the ingestion of gluten-containing cereals, have been increasing in prevalence. Patients with celiac disease have gluten-specific immune responses, but the contribution of non-gluten proteins to symptoms in patients with celiac disease or other wheat-related disorders is controversial. Methods C57BL/6 (control), Myd88–/–, Ticam1–/–, and Il15–/– mice were placed on diets that lacked wheat or gluten, with or without wheat amylase trypsin inhibitors (ATIs), for 1 week. Small intestine tissues were collected and intestinal intraepithelial lymphocytes (IELs) were measured; we also investigated gut permeability and int…

0301 basic medicineInflammationdigestive systemSensitivity and SpecificityGliadin03 medical and health sciencesDiet Gluten-FreeMiceRandom Allocation0302 clinical medicineImmune systemReference ValuesLactobacillusmedicineAnimalsHumansAmylaseTriticum2. Zero hungerchemistry.chemical_classificationToll-like receptorHepatologybiologybusiness.industryGastroenterologynutritional and metabolic diseasesbiology.organism_classificationGlutendigestive system diseasesSmall intestineImmunity Innate3. Good healthGastrointestinal MicrobiomeMice Inbred C57BLCeliac DiseaseDisease Models AnimalLactobacillus030104 developmental biologymedicine.anatomical_structurechemistryImmunologyAmylasesbiology.proteinIntraepithelial lymphocyte030211 gastroenterology & hepatologymedicine.symptombusinessTrypsin InhibitorsGastroenterology
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The Ciona intestinalis immune-related galectin genes (CiLgals-a and CiLgals-b) are expressed by the gastric epithelium.

2017

The transcription of two Ciona intestinalis galectin genes (CiLgals-a and CiLgalseb) is uparegulated by LPS in the pharynxis (hemocytes, vessel epithelium, endostilar zones) which is retained the main organ of the immunity. In this ascidian, for the first time we show, by immunohistochemistry and in situ hybridization methods, that these two immune-related genes are expressed in the gastric epithelium of naïve ascidians, whereas the galectins appear to be only contained in the intestine columnar epithelium. In addition, according to previous results on the pharynx, the genes are also expressed and galectins produced by hemocytes scattered in the connective tissue surrounding the gut. The ge…

0301 basic medicineLipopolysaccharidesPathologymedicine.medical_specialtyanimal structuresGalectinsSettore BIO/05 - ZoologiaConnective tissueIn situ hybridizationAquatic Science03 medical and health sciencesDownregulation and upregulationGene expressionotorhinolaryngologic diseasesmedicineGalectin genes expression Ascidians Ciona intestinalis Gastric and intestine epithelia Hemocytes in the connective tissue Immunolocalization In situ hybridizationEnvironmental ChemistryAnimalsCiona intestinalisIntestinal MucosaGeneIn Situ HybridizationGalectin030102 biochemistry & molecular biologybiologyGeneral Medicinebiology.organism_classificationImmunohistochemistryEpitheliumCell biologyCiona intestinalis030104 developmental biologymedicine.anatomical_structurePharynxFishshellfish immunology
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Evidence of Absorptive Function in vivo in a Neo-Formed Bio-Artificial Intestinal Segment Using a Rodent Model.

2015

A promising therapeutic approach for intestinal failure consists in elongating the intestine with a bio-engineered segment of neo-formed autologous intestine. Using an acellular biologic scaffold (ABS), we, and others, have previously developed an autologous bio-artificial intestinal segment (BIS) that is morphologically similar to normal bowel in rodents. This neo-formed BIS is constructed with the intervention of naïve stem cells that repopulate the scaffold in vivo, and over a period of time, are transformed in different cell populations typical of normal intestinal mucosa. However, no studies are available to demonstrate that such BIS possesses functional absorptive characteristics nece…

0301 basic medicineMalePathologymedicine.medical_specialtyCell typeLumen (anatomy)Bio-artificial intestineBio-engineered intestineIntestinal absorption03 medical and health sciences0302 clinical medicineIntestinal mucosaIn vivoIntestine SmallmedicineAnimalsIntestinal MucosabiologyBioartificial OrgansTissue EngineeringTissue ScaffoldsIn vivo absorptionGastroenterologyCystic fibrosis transmembrane conductance regulatorRatsFunctional analysis of bio-artificial intestine030104 developmental biologyIntestinal Absorptionbiology.proteinUltrastructure030211 gastroenterology & hepatologySurgeryStem cellJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
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Taeniasis vs cysticercosis infection routes

2016

Although cysticercosis caused by Taenia solium ( T. soliu ) is considered a neglected disease, its life cycle has been well known for more than two centuries. T. solium not only causes cysticercosis but also taeniasis in humans. These two diseases have totally different infection routes. To acquire taeniasis (the presence of the adult stage of T. solium in the intestine), humans have to ingest the larval stage (cysticercus) that infects a variety of organs and viscera in pigs, its intermediate hosts. Therefore, taeniasis is acquired when eating raw or undercooked infected pork. The adult stage in the human intestine release eggs that contain a hexacanth embryo, the oncosphere. If humans acc…

0301 basic medicineMedicine(all)Human intestine030231 tropical medicineNeglected DiseaseOncospherePhysiologyCysticercusCysticercosisGeneral Medicine030108 mycology & parasitologyBiologymedicine.disease03 medical and health sciencesmedicine.drug_formulation_ingredient0302 clinical medicineImmunologyTaenia soliumparasitic diseasesmedicineIngestionTaeniasisAsian Pacific Journal of Tropical Medicine
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