Search results for "toll"

showing 10 items of 324 documents

Gut microbiota regulate hepatic von Willebrand factor synthesis and arterial thrombus formation via Toll-like receptor-2.

2016

The symbiotic gut microbiota play pivotal roles in host physiology and the development of cardiovascular diseases, but the microbiota-triggered pattern recognition signaling mechanisms that impact thrombosis are poorly defined. In this article, we show that germ-free (GF) and Toll-like receptor-2 (Tlr2)-deficient mice have reduced thrombus growth after carotid artery injury relative to conventionally raised controls. GF Tlr2-/- and wild-type (WT) mice were indistinguishable, but colonization with microbiota restored a significant difference in thrombus growth between the genotypes. We identify reduced plasma levels of von Willebrand factor (VWF) and reduced VWF synthesis, specifically in he…

0301 basic medicineBlood Plateletsmedicine.medical_specialtyEndotheliumPlatelet AggregationImmunologyBiologyBiochemistry03 medical and health sciencesMiceVon Willebrand factorhemic and lymphatic diseasesInternal medicinevon Willebrand FactormedicineAnimalsGerm-Free LifePlateletThrombusIntegrin bindingMice KnockoutToll-like receptorThrombosisCell BiologyHematologymedicine.diseaseToll-Like Receptor 2Gastrointestinal MicrobiomeTLR2030104 developmental biologymedicine.anatomical_structureEndocrinologyLivercardiovascular systembiology.proteinSignal transductioncirculatory and respiratory physiologySignal TransductionBlood
researchProduct

TlR expression profile of human gingival margin-derived stem progenitor cells

2015

Background Gingival margin-derived stem/progenitor cells (G-MSCs) show remarkable periodontal regenerative potential in vivo. During regeneration, G-MSCs may interact with their inflammatory environment via toll-like-receptors (TLRs). The present study aimed to depict the G-MSCs TLRs expression profile. Material and Methods Cells were isolated from free gingival margins, STRO-1-immunomagnetically sorted and seeded to obtain single colony forming units (CFUs). G-MSCs were characterized for CD14, CD34, CD45, CD73, CD90, CD105, CD146 and STRO-1 expression, and for multilineage differentiation potential. Following G-MSCs’ incubation in basic or inflammatory medium (IL-1β, IFN-γ, IFN-α, TNF-α) a…

0301 basic medicineCD14GingivaCD34OdontologíaBiology03 medical and health sciencesHumansCD90Progenitor cellGeneral DentistryCells CulturedColony-forming unitOral Medicine and PathologyStem CellsResearchRegeneration (biology)Toll-Like Receptors:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludCell biology030104 developmental biologyOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASImmunologyCD146SurgeryStem cellMedicina Oral Patología Oral y Cirugia Bucal
researchProduct

Imiquimod inhibits growth and induces differentiation of myeloid leukemia cell lines

2018

Background: The antitumoral effects of different Toll-like receptor (TLRs) agonists is mediated by activating immune responses to suppress tumors growth, although TLR ligands may also have a direct effect on tumoral cells. Given that TLR signaling induces hematopoietic cell differentiations this may serve as a novel differentiation therapeutic approach for AML. Methods: We investigated the effects of agonists for the ten human TLRs on the proliferation, apoptosis, cell cycle and differentiation of ten different types of myeloid leukemia cell lines (HL-60, U-937, KG-1, KG-1a, K-562, Kasumi-1, EOL-1, NB4, MOLM-13 and HEL). Proliferation was measured using the CellTiter 96 (R) Aqueous One Solu…

0301 basic medicineCancer ResearchMyeloidImiquimodlcsh:RC254-282Flow cytometry03 medical and health sciences0302 clinical medicineToll-like receptorGeneticsmedicineCytotoxic T cellMyeloid leukemia cell lineslcsh:QH573-671Toll-like receptorImiquimodmedicine.diagnostic_testChemistryCell growthlcsh:CytologyMyeloid leukemiaCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchPrimary Researchmedicine.drugCancer Cell International
researchProduct

Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

2019

Summary MyD88, an adaptor molecule downstream of innate pathways, plays a significant tumor-promoting role in sporadic intestinal carcinogenesis of the Apcmin/+ model, which carries a mutation in the Apc gene. Here, we show that deletion of MyD88 in intestinal mesenchymal cells (IMCs) significantly reduces tumorigenesis in this model. This phenotype is associated with decreased epithelial cell proliferation, altered inflammatory and tumorigenic immune cell infiltration, and modified gene expression similar to complete MyD88 knockout mice. Genetic deletion of TLR4, but not interleukin-1 receptor (IL-1R), in IMCs led to altered molecular profiles and reduction of intestinal tumors similar to …

0301 basic medicineCarcinogenesisBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciences0302 clinical medicinemedicinetumor microenvironmentAnimalsHumansReceptorinnate immunityTumor microenvironmentInnate immune systemMesenchymal stem cellCell biologyIntestinesToll-Like Receptor 4030104 developmental biologyMyeloid Differentiation Factor 88Knockout mouseTLR4Carcinogenesiscancer-associated fibroblasts030217 neurology & neurosurgerySignal Transduction
researchProduct

Extracellular histones activate autophagy and apoptosis via mTOR signaling in human endothelial cells.

2018

Circulating histones have been proposed as targets for therapy in sepsis and hyperinflammatory symptoms. However, the proposed strategies have failed in clinical trials. Although different mechanisms for histone-related cytotoxicity are being explored, those mediated by circulating histones are not fully understood. Extracellular histones induce endothelial cell death, thereby contributing to the pathogenesis of complex diseases such as sepsis and septic shock. Therefore, the comprehension of cellular responses triggered by histones is capital to design effective therapeutic strategies. Here we report how extracellular histones induce autophagy and apoptosis in a dose-dependent manner in cu…

0301 basic medicineCell SurvivalEndothelial cellsFisiologiaApoptosisAMP-Activated Protein KinasesHistones03 medical and health sciencesExtracellularAutophagyHuman Umbilical Vein Endothelial CellsAutophagy-Related Protein-1 HomologHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologyDose-Response Relationship DrugChemistryTOR Serine-Threonine KinasesAutophagyIntracellular Signaling Peptides and ProteinsAMPKNuclear ProteinsCirculating histonesCell biologyToll-like receptorsEndothelial stem cell030104 developmental biologyHistoneApoptosisbiology.proteinMolecular MedicineProto-Oncogene Proteins c-aktSignal TransductionBiochimica et biophysica acta. Molecular basis of disease
researchProduct

Mast cells within cellular networks

2018

Mast cells are highly versatile in terms of their mode of activation by a host of stimuli and their ability to flexibly release a plethora of biologically highly active mediators. Within the immune system, mast cells can best be designated as an active nexus interlinking innate and adaptive immunity. Here we try to draw an arc from initiation of acute inflammatory reactions to microbial pathogens to development of adaptive immunity and allergies. This multifaceted nature of mast cells is made possible by interaction with multiple cell types of immunologic and nonimmunologic origin. Examples for the former include neutrophils, eosinophils, T cells, and professional antigen-presenting cells. …

0301 basic medicineCell typeSensory Receptor CellsNeutrophilsT-LymphocytesImmunologyAntigen-Presenting CellsCell CommunicationAdaptive Immunity03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansImmunology and AllergyMast CellsAntigen-presenting cellToll-like receptorMHC class IIbiologyAcquired immune systemMast cellAsthmaImmunity InnateEosinophilsCrosstalk (biology)030104 developmental biologymedicine.anatomical_structureImmunologybiology.protein030215 immunologyJournal of Allergy and Clinical Immunology
researchProduct

CD14 is a key organizer of microglial responses to CNS infection and injury

2015

Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon β-mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced …

0301 basic medicineChemokineToll-like receptorInnate immune systembiologyMicrogliaCD14Proinflammatory cytokine03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologymedicine.anatomical_structureImmune systemNeurologyImmunologybiology.proteinTLR4medicineGlia
researchProduct

Toll-like receptors in neuroinflammation, neurodegeneration, and alcohol-induced brain damage

2021

Toll-like receptors (TLRs) or pattern recognition receptors respond to pathogen-associated molecular patterns (PAMPs) or internal damage-associated molecular patterns (DAMPs). TLRs are integral membrane proteins with both extracellular leucine-rich and cytoplasmic domains that initiate downstream signaling through kinases by activating transcription factors like AP-1 and NF-κB, which lead to the release of various inflammatory cytokines and immune modulators. In the central nervous system, different TLRs are expressed mainly in microglia and astroglial cells, although some TLRs are also expressed in oligodendroglia and neurons. Activation of TLRs triggers signaling cascades by the host as a…

0301 basic medicineClinical BiochemistryActivating transcription factorGene ExpressionBiologyExosomesBiochemistryProinflammatory cytokine03 medical and health sciences0302 clinical medicineImmune systemGeneticsmedicineAnimalsHumansReceptorMolecular BiologyNeuroinflammationMicrogliaToll-Like ReceptorsNeurodegenerationPattern recognition receptorBrainNeurodegenerative DiseasesCell Biologymedicine.diseaseImmunity InnateCell biologyAlcoholismMicroRNAs030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisNeuroinflammatory Diseases
researchProduct

1-ethyl-3-(6-methylphenanthridine-8-il) urea modulates TLR3/9 activation and induces selective pro-inflammatory cytokine expression in vitro.

2017

We have previously demonstrated the nucleic acid binding capacity of phenanthridine derivatives (PHTs). Because nucleic acids are potent inducers of innate immune response through Toll-like receptors (TLRs), and because PTHs bear a structural resemblance to commonly used synthetic ligands for TLR7/8, we hypothesized that PHTs could modulate/activate immune response. We found that compound M199 induces secretion of IL-6, IL-8 and TNFα in human PBMCs and inhibits TLR3/9 activation in different cellular systems (PBMCs, HEK293 and THP-1 cell lines).

0301 basic medicineClinical BiochemistryPharmaceutical ScienceDown-RegulationBiochemistryCell Line03 medical and health sciences0302 clinical medicineImmune systemDrug DiscoveryHumansImmunologic FactorsUreaSecretionReceptorMolecular BiologyInnate immune systemChemistryInterleukin-6Tumor Necrosis Factor-alphaOrganic ChemistryInterleukin-8Interferon-alphaTLR7Molecular biologyphenantridines ; TLR ; PBMCs ; cytokines ; immunomodulationIntercalating AgentsPhenanthridinesToll-Like Receptor 3030104 developmental biologyOligodeoxyribonucleotidesToll-Like Receptor 9TLR3Nucleic acidMolecular MedicineTumor necrosis factor alpha030215 immunologySignal TransductionBioorganicmedicinal chemistry letters
researchProduct

Gut microbiota imbalance and colorectal cancer

2016

International audience; The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes (e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the g…

0301 basic medicineColorectal cancer[SDV]Life Sciences [q-bio]enterotoxigenic bacteroides-fragilisGut floraCyclomodulin[ SDV.CAN ] Life Sciences [q-bio]/CancerTopic Highlightstreptococcus-gallolyticus infectionbiologyGastrointestinal MicrobiomeGastroenterologyGeneral Medicinecytolethal-distending toxin3. Good healthlactobacillus-acidophilus deficientIntestinesCell Transformation NeoplasticHost-Pathogen InteractionsInflammation MediatorsColorectal NeoplasmsVirulence Factorspolymerase-chain-reaction[SDV.CAN]Life Sciences [q-bio]/CancerGut microbiotaoxidative dna-damageMicrobiologyescherichia-coli strains03 medical and health scienceshelicobacter-pylori infectionmedicineAnimalsHumansMicrobiomeBacteria[ SDV ] Life Sciences [q-bio]inflammatory-bowel-diseaseCancerHelicobacter pyloribiology.organism_classificationmedicine.diseaseStreptococcus bovisColorectal cancerGastrointestinal MicrobiomeHépatologie et Gastroentérologie030104 developmental biologytoll-like receptorsOxidative stressImmunologyHépatology and GastroenterologyDysbiosiscolorectal cancer;gut microbiota;dysbiosis;cyclomodulin;oxidative;stress;enterotoxigenic bacteroides-fragilis;oxidative dna-damage;cytolethal-distending toxin;inflammatory-bowel-disease;streptococcus-gallolyticus infection;lactobacillus-acidophilus;deficient;helicobacter-pylori infection;polymerase-chain-reaction;escherichia-coli strains;toll-like receptorsDysbiosisDNA Damage
researchProduct