0000000000319653

AUTHOR

Nadine Wittkopf

showing 4 related works from this author

Assessment of Tumor Development and Wound Healing Using Endoscopic Techniques in Mice

2010

Mouse models of intestinal inflammation and colon cancer are valuable tools to gain insights into the pathogenesis of the corresponding human diseases. Recently, in vivo mouse endoscopy has been developed, allowing not only the high-resolution monitoring and scoring of experimental disease development, but also enables the investigator to perform manipulations, including local injection of reagents or the taking of biopsies for molecular and histopathologic analyses. Chromoendoscopic staining with methylene blue enables visualization of the crypt structure and allows discrimination between inflammatory and neoplastic changes. The development of endoscopic techniques in live mice opened new …

Pathologymedicine.medical_specialtyColorectal cancerBiopsyDiseasePathogenesisMiceMicromanipulation03 medical and health sciences0302 clinical medicineIn vivoIntestinal inflammationmedicineAnimalsHumans030304 developmental biologyWound Healing0303 health sciencesMiniaturizationHepatologymedicine.diagnostic_testbusiness.industryDisease mechanismsGastroenterologyEndoscopyColitismedicine.disease3. Good healthEndoscopyEndoscopes GastrointestinalDisease Models AnimalColonic Neoplasms030211 gastroenterology & hepatologybusinessWound healingGastroenterology
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STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing.

2009

Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific d…

STAT3 Transcription FactorAnimals; Colitis/chemically induced; Colitis/immunology; Dextran Sulfate/pharmacology; Epithelial Cells/cytology; Epithelial Cells/physiology; Gene Expression Profiling; Inflammation/immunology; Inflammation/pathology; Interleukin-6/genetics; Interleukin-6/immunology; Interleukins/genetics; Interleukins/immunology; Intestinal Mucosa/cytology; Intestinal Mucosa/pathology; Mice; Mice Inbred C57BL; Mice Knockout; Oligonucleotide Array Sequence Analysis; STAT3 Transcription Factor/genetics; STAT3 Transcription Factor/metabolism; Signal Transduction/physiology; Wound HealingImmunologyInterleukin 22Mice03 medical and health sciences0302 clinical medicineIntestinal mucosaConditional gene knockoutImmunology and AllergyAnimalsIntestinal MucosaSTAT3Oligonucleotide Array Sequence Analysis030304 developmental biologyInflammationMice KnockoutWound Healing0303 health sciencesbiologyInterleukin-6Gene Expression ProfilingInterleukinsDextran SulfateBrief Definitive ReportEpithelial CellsCell BiologySTAT3 Transcription FactorColitisIntestinal epithelium3. Good healthMice Inbred C57BLbiology.proteinCancer researchSTAT proteinWound healingSignal Transduction030215 immunology
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Caspase-8 regulates TNF-alpha induced epithelial necroptosis and terminal ileitis

2011

Two groups identify the regulation of death-receptor-induced necroptosis as an epithelial intrinsic mechanism that is important for the maintenance of immune homeostasis and the prevention of intestinal inflammation in mice. Welz et al. describe an unexpected physiological function for FADD (Fas-associated protein with death domain), an adaptor protein required for death-receptor-induced apoptosis. Mice with intestinal epithelial specific knockout of FADD develop severe colon inflammation due to increased death of FADD-deficient colonic epithelial cells. Gunther et al. report a novel and unexpected function of caspase-8 in maintaining immune homeostasis in the gut. Caspase-8 expression by g…

Programmed cell deathPaneth CellsNecroptosisInflammationApoptosisBiologyIn Vitro Techniquesdigestive systemArticle03 medical and health sciencesMiceNecrosis0302 clinical medicineCrohn DiseasemedicineAnimalsHumansFADD030304 developmental biology0303 health sciencesCaspase 8MultidisciplinaryInnate immune systemTumor Necrosis Factor-alphaColitisIntestinal epithelium3. Good healthmedicine.anatomical_structure030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesPaneth cellImmunologybiology.proteinCancer researchTumor necrosis factor alphaGoblet Cellsmedicine.symptomGene DeletionNature
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Activation of Intestinal Epithelial Stat3 Orchestrates Tissue Defense during Gastrointestinal Infection

2015

Gastrointestinal infections with EHEC and EPEC are responsible for outbreaks of diarrheal diseases and represent a global health problem. Innate first-line-defense mechanisms such as production of mucus and antimicrobial peptides by intestinal epithelial cells are of utmost importance for host control of gastrointestinal infections. For the first time, we directly demonstrate a critical role for Stat3 activation in intestinal epithelial cells upon infection of mice with Citrobacter rodentium - a murine pathogen that mimics human infections with attaching and effacing Escherichia coli. C. rodentium induced transcription of IL-6 and IL-22 in gut samples of mice and was associated with activat…

STAT3 Transcription FactorColonAntimicrobial peptideslcsh:MedicineInflammation-digestive systemMicrobiologyMiceMedizinische FakultätmedicineCitrobacter rodentiumAnimalsHumansddc:610Intestinal Mucosalcsh:ScienceSTAT3PathogenMice KnockoutGastrointestinal tractMultidisciplinarybiologylcsh:REnterobacteriaceae InfectionsEpithelial CellsColitisMucusEpitheliumIntestinesMice Inbred C57BLmedicine.anatomical_structureImmunologybiology.proteinCitrobacter rodentiumlcsh:Qmedicine.symptomResearch ArticlePLoS ONE
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