Search results for "TLR4"

showing 10 items of 96 documents

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
researchProduct

TLR4 polymorphisms and ageing: implications for the pathophysiology of age-related diseases.

2009

Innate immunity provides a first line of host defense against infection by recognizing and killing microbes while simultaneously activating an instructive immune response. Toll-like receptors (TLRs) are principal mediators of rapid microbial recognition and function mainly by detection of pathogen-associated molecular patterns that do not exist in the host. Recognition of their ligands leads to a series of signaling events resulting in acute host responses, involved in killing pathogens. Discussion We describe the involvement of TLR4 polymorphisms in ageing, and in particular in age-related diseases, suggesting the crucial role of molecules of innate immunity in pathophysiology of these dis…

Malemedicine.medical_specialtyAgingImmunologyLongevitySNPBiologyPolymorphism Single NucleotideatherosclerosiImmune systemMedical microbiologyAlzheimer DiseasemedicinecancerImmunology and AllergyHumansGenetic Predisposition to DiseaseTLR4Receptorinnate immunityAllelesSettore MED/04 - Patologia GeneraleInnate immune systemHost (biology)Prostatic Neoplasmsmedicine.diseaseImmunity InnateToll-Like Receptor 4AgeingCardiovascular DiseasesImmunologyTLR4FemaleAlzheimer's diseaseAlzheimer’s diseaseFunction (biology)Journal of clinical immunology
researchProduct

Toll-like receptor 2 mediates prostaglandin E2 production in murine peritoneal macrophages and splenocytes in response to Candida albicans

2004

The involvement of Toll-like receptor 2 (TLR2) and TLR4 in triggering signal transduction pathways leading to prostaglandin E(2) (PGE(2)) production in response to Candida albicans has been studied in cells from wild-type, TLR2-/- and TLR4-/- knockout mice. In vitro PGE(2) production by macrophages challenged with zymosan, yeast or hypha cells was strongly inhibited in TLR2-deficient cells, but not in TLR4-/- cells, as compared to macrophages from wild-type mice. PGE(2) production was dependent on de novo cyclooxygenase-2 (Cox2) synthesis, since unchallenged cells failed to produce PGE(2) and specific Cox2 inhibition during challenge totally blocked PGE(2) production. Similar results were o…

Malemedicine.medical_treatmentReceptors Cell SurfaceBiologyMicrobiologyDinoprostoneMicechemistry.chemical_compoundCandida albicansmedicineAnimalsProstaglandin E2Candida albicansMolecular BiologyCells CulturedMice KnockoutToll-like receptorZymosanGeneral Medicinebiology.organism_classificationMolecular biologyToll-Like Receptor 2Corpus albicansToll-Like Receptor 4TLR2chemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesImmunologyMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Signal Transductionmedicine.drugProstaglandin EResearch in Microbiology
researchProduct

Human toll-like receptor 4 mutations are associated with susceptibility to invasive meningococcal disease in infancy.

2006

Toll-like receptor 4 (TLR4) is required for efficient recognition of bacterial infections. We investigated an association between 2 TLR4 mutations (Asp 299 Gly and Thr 399 Ile) and meningococcal disease in 197 patients and 214 healthy controls by allele-specific real time polymerase chain reaction and direct sequencing. Although the allele frequency was not higher in the overall patient population, a significantly higher frequency in the 40 patients younger than 12 months of age (P = 0.007) was observed. We conclude that TLR4 mutations represent a risk factor for meningococcal disease in this age group.

Microbiology (medical)MaleMutation MissenseMeningococcal diseasemedicine.disease_causePolymerase Chain ReactionGene FrequencyMedicineHumansGenetic Predisposition to DiseaseRisk factorReceptorChildAllele frequencyAllelesToll-like receptorMutationbusiness.industryAge FactorsInfantDNASequence Analysis DNAmedicine.diseaseEuropeMeningococcal InfectionsToll-Like Receptor 4Infectious DiseasesReal-time polymerase chain reactionAmino Acid SubstitutionChild PreschoolPediatrics Perinatology and Child HealthImmunologyTLR4FemalebusinessThe Pediatric infectious disease journal
researchProduct

About the role of TLR2 and TLR4 in cytokine secretion by murine macrophages in response to Candida albicans.

2006

Dear Editor, In a recent issue of FEMS Immunology and Medical Microbiology , Blasi (2005) studied the biological role of Toll-like receptor (TLR)2 and TLR4 in the effector and secretory responses of murine macrophages to the fungal species Candida albicans . In their article, the authors conclude that the secretory response to C. albicans appears to be TLR4- but not TLR2-dependent. In our opinion this statement is misleading as the results reported do not support this conclusion and, therefore, we wish to comment on this issue. There is evidence indicating that TLR2 is the main receptor involved in triggering cytokine production by murine macrophages in response to C. albicans . Phospholipo…

Microbiology (medical)medicine.medical_treatmentImmunologyMicrobiologyMicrobiologyMiceCandida albicansmedicineImmunology and AllergyAnimalsCandida albicansbiologyEffectorMacrophagesCandidiasisGeneral Medicinebiology.organism_classificationCorpus albicansToll-Like Receptor 2Toll-Like Receptor 4TLR2Infectious DiseasesCytokineImmunologyTLR4CytokinesCytokine secretionTumor necrosis factor alphaFEMS immunology and medical microbiology
researchProduct

Signaling pathways of the TREM-1- and TLR4-mediated neutrophil oxidative burst.

2008

The triggering receptor expressed on myeloid cells 1 (TREM-1) is involved in the innate inflammatory response to microbial infections. Activation and expression of TREM-1 by polymorphonuclear neutrophils (PMN) occurs in concert with Toll-like receptors (TLR) such as TLR4 for bacterial lipopolysaccharide. However, it is currently unclear how this is mediated on a molecular level. Using pharmacological inhibitors and Western blot analysis we demonstrate that phosphatidyl inositide 3-kinase, phospholipase C and the mitogen-activated kinase p38MAPK are essential for the TREM-1- and TLR4-induced oxidative burst of human PMN. The activation of protein kinase B and extracellular signal-related kin…

Models MolecularLipopolysaccharideNeutrophilsBlotting WesternCell Separationp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundPhosphatidylinositol 3-KinasesImmunology and AllergyHumansReceptors ImmunologicReceptorProtein kinase BRespiratory BurstMembrane GlycoproteinsPhospholipase CKinaseFlow CytometryTriggering Receptor Expressed on Myeloid Cells-1Respiratory burstCell biologyEnzyme ActivationToll-Like Receptor 4chemistryTLR4Signal transductionProto-Oncogene Proteins c-aktSignal TransductionJournal of innate immunity
researchProduct

Inflammation events occurring upon bacterial infection in Mytilus galloprovincialis

2022

Bivalves, and in particular the Mediterranean Mytilus galloprovincialis are important sources of food in several countries in the world. Because of that, mussels farming has a strong economic impact. Due to their status as sessile and filter-feeding animals, bivalves accumulate in their tissues environmental pollutants and a larger amount of microorganisms and between these, a multitude of infective bacteria for higher vertebrates and humans, such as Vibrio species. Several immunological responses of M. galloprovincialis were investigated and described after Vibrio infection both, in vitro and in vivo conditions, such as hemocytes count and different cellular subpopulations. Particularly, i…

Mytilus TLR4 MYD88 AIF1 RNASET2 Vibrio infection
researchProduct

AIF-1 and RNASET2 are involved in the inflammatory response in the Mediterranean mussel Mytilus galloprovincialis following Vibrio infection

2022

Filter-feeding bivalves, such as the Mytilus species, are exposed to different types of bacteria in the surrounding waters, in particular of the Vibrio genus. Mussels lack an adaptive immune system and hemocytes can recognize pathogen-associated molecular patterns (PAMPs) via pattern recognition receptors (PRRs) to activate intracellular signaling pathways to trigger the antimicrobial effectors synthesis. Among the areas of bivalve immunity that deserve study include the role of hemocyte subpopulations. Since little information are available on immune responses at the tissue level to human pathogenic vibrios commonly detected in coastal waters involved in seafood-borne diseases, in this wor…

MytilusHemocytesTumor Suppressor ProteinsAIF-1 Bacterial challenge Cellular immunity Immunohistochemistrym M. galloprovincialis Myd88 RNASET2 TLR4RNASET2General MedicineAquatic ScienceAIF-1; Bacterial challenge; Cellular immunity; Immunohistochemistry; M. galloprovincialis; Myd88; RNASET2; TLR4Myd88ImmunohistochemistryCellular immunityToll-Like Receptor 4Bacterial challengeRibonucleasesSeafoodVibrio InfectionsMyeloid Differentiation Factor 88Environmental ChemistryAnimalsHumansTLR4M. galloprovincialisAIF-1Vibrio
researchProduct

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
researchProduct

TLR4 abrogates the Th1 immune response through IRF1 and IFN-β to prevent immunopathology during L. infantum infection

2020

A striking feature of human visceral leishmaniasis (VL) is chronic inflammation in the spleen and liver, and VL patients present increased production levels of multiple inflammatory mediators, which contribute to tissue damage and disease severity. Here, we combined an experimental model with the transcriptional profile of human VL to demonstrate that the TLR4-IFN-β pathway regulates the chronic inflammatory process and is associated with the asymptomatic form of the disease. Tlr4-deficient mice harbored fewer parasites in their spleen and liver than wild-type mice. TLR4 deficiency enhanced the Th1 immune response against the parasite, which was correlated with an increased activation of de…

PhysiologyGene ExpressionWhite Blood CellsMiceCell SignalingAnimal CellsImmune PhysiologyZoonosesImmunopathologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Immune ResponseLeishmaniasisProtozoansLeishmaniaMice Knockout0303 health sciencesbiologyT Cells030302 biochemistry & molecular biologyEukaryotaImmune Receptor SignalingInfectious Diseasesmedicine.anatomical_structureLeishmaniasis VisceralCellular Typesmedicine.symptomLeishmania infantumResearch ArticleSignal TransductionNeglected Tropical DiseasesQH301-705.5Leishmania InfantumImmune CellsImmunologySpleenInflammationLEISHMANIOSE VISCERALMicrobiology03 medical and health sciencesImmune systemVirologyParasitic DiseasesGeneticsmedicineAnimalsMolecular Biology030304 developmental biologyInflammationProtozoan InfectionsBlood CellsOrganismsBiology and Life SciencesCell BiologyInterferon-betaTh1 CellsRC581-607Tropical Diseasesmedicine.diseasebiology.organism_classificationParasitic ProtozoansToll-Like Receptor 4IRF1Visceral leishmaniasisImmunologyTLR4ParasitologyImmunologic diseases. AllergySpleenInterferon Regulatory Factor-1
researchProduct