0000000000267081

AUTHOR

Julia-stefanie Frick

0000-0002-7662-7956

showing 3 related works from this author

Steady-state neutrophil homeostasis is dependent on TLR4/TRIF signaling

2013

Polymorphonuclear neutrophil granulocytes (neutrophils) are tightly controlled by an incompletely understood homeostatic feedback loop adjusting the marrow's supply to peripheral needs. Although it has long been known that marrow cellularity is inversely correlated with G-CSF levels, the mechanism linking peripheral clearance to production remains unknown. Herein, the feedback response to antibody induced neutropenia is characterized to consist of G-CSF–dependent shifts of marrow hematopoietic progenitor populations including expansion of the lin-/Sca-1/c-kit (LSK) and granulocyte macrophage progenitor (GMP) compartments at the expense of thrombopoietic and red cell precursors. Evidence is …

NeutrophilsImmunologyRecombinant Granulocyte Colony-Stimulating FactorBiologyBiochemistryGranulopoiesisMiceGranulocyte Colony-Stimulating FactorAnimalsHomeostasisGranulocyte Precursor CellsLymphocytesNeutrophil homeostasisReceptorMice KnockoutCell BiologyHematologyGranulocyte colony-stimulating factorToll-Like Receptor 4Adaptor Proteins Vesicular TransportTRIFMyeloid Differentiation Factor 88ImmunologyTLR4HomeostasisSignal TransductionBlood
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Wheat Consumption Aggravates Colitis in Mice via Amylase Trypsin Inhibitor–mediated Dysbiosis

2020

Background & Aims Wheat has become the world's major staple and its consumption correlates with prevalence of noncommunicable disorders such as inflammatory bowel diseases. Amylase trypsin inhibitors (ATIs), a component of wheat, activate the intestine's innate immune response via toll-like receptor 4 (TLR4). We investigated the effects of wheat and ATIs on severity of colitis and fecal microbiota in mice. Methods C57BL/6 wild-type and Tlr4–/– mice were fed wheat- or ATI-containing diets or a wheat-free (control) diet and then given dextran sodium sulfate to induce colitis; we also studied Il10–/– mice, which develop spontaneous colitis. Changes in fecal bacteria were assessed by taxa-speci…

MaleTrypsin inhibitorPlant Proteins DietarySeverity of Illness IndexInflammatory bowel diseaseMicrobiologyFecesMicemedicineAnimalsHumansAmylaseColitisTriticumFecesMice KnockoutHepatologybiologyDextran SulfateGastroenterologyfood and beveragesFecal Microbiota TransplantationColitisInflammatory Bowel Diseasesmedicine.diseaseAnimal FeedImmunity InnateGastrointestinal MicrobiomeToll-Like Receptor 4TransplantationDisease Models Animalbiology.proteinTLR4DysbiosisTrypsin InhibitorsDysbiosisSignal TransductionGastroenterology
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Bacteroides vulgatus protects against escherichia coli-induced colitis in gnotobiotic interleukin-2-deficient mice

2003

Abstract Background & Aims: The microflora plays a crucial role in inflammatory bowel diseases (IBDs). Specific pathogen-free (SPF), but not germ-free, interleukin (IL)-2-deficient (IL-2−/−) mice develop colitis. The colitogenicity of commensal bacteria was determined. Methods: Gnotobiotic IL-2−/− and IL-2+/+ mice were colonized with Escherichia coli mpk, Bacteroides vulgatus mpk, or both bacterial strains, or with E. coli strain Nissle 1917. DNA arrays were used to characterize E. coli mpk. Colitis was analyzed by histology and real-time reverse-transcription polymerase chain reaction (RT-PCR) for interferon (IFN)-γ, tumor necrosis factor (TNF)-α, IL-10, and CD14 messenger RNA (mRNA) expre…

MaleGene Expressionmedicine.disease_causeMicrobiologyFecesMiceInterferonEscherichia colimedicineAnimalsBacteroidesGerm-Free LifeColitisEscherichia coliBacteroidaceaeEscherichia coli InfectionsSpecific-pathogen-freeHepatologybiologyGastroenterologyInterleukinColitismedicine.diseasebiology.organism_classificationEnterobacteriaceaeMice Mutant StrainsSpecific Pathogen-Free OrganismsIntestinesMice Inbred C57BLInterleukin-2FemaleTumor necrosis factor alphamedicine.drugGastroenterology
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