Search results for "INNATE IMMUNITY"

showing 10 items of 115 documents

Inflamed adult pharynx tissues and swimming larva of Ciona intestinalis share CiTNFalpha-producing cells.

2010

In situ hybridisation and immunohistochemistry analyses have shown that the Ciona intestinalis tumour necrosis factor alpha gene (CiTNFalpha), which has been previously cloned and sequenced, is expressed either during the inflammatory pharynx response to lipopolysaccharide (LPS) or during the swimming larval phase of development. Granulocytes with large granules and compartment/morula cells are CiTNFalpha-producing cells in both inflamed pharynx and larvae. Pharynx vessel endothelium also takes part in the inflammatory response. Haemocyte nodules in the vessel lumen or associated with the endothelium suggest the involvement of CiTNFalpha in recruiting lymphocyte-like cells and promoting the…

LipopolysaccharidesPathologymedicine.medical_specialtyHistologyHemocytesEndotheliumEvolutionMesenchymeSettore BIO/05 - ZoologiaInflammationIn situ hybridizationBiologyAscidia Ciona intestinalisPathology and Forensic MedicinemedicineAnimalsCiona intestinalisTumour necrosis factor; Pharynx; Inflammation; Haemocytes; Larval development; Innate immunity; Evolution; Ascidia Ciona intestinalisIn Situ Hybridization FluorescencePhylogenyInflammationInnate immunityInnate immune systemTumor Necrosis Factor-alphaPharynxMetamorphosis BiologicalHaemocytePharyngitisCell Biologybiology.organism_classificationImmunohistochemistryCiona intestinalismedicine.anatomical_structureLarval developmentLarvaImmunohistochemistryPharynxmedicine.symptomTumour necrosis factorGranulocytesCell and tissue research
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LPS challenge regulates gene expression and tissue localization of a Ciona intestinalis gene through an alternative polyadenylation mechanism.

2013

A subtractive hybridization strategy for the identification of differentially expressed genes was performed between LPS-challenged and naive Ciona intestinalis. This strategy allowed the characterization of two transcripts (Ci8short and Ci8long) generated by the use of two Alternative Polyadenylation sites. The Ci8long transcript contains a protein domain with relevant homology to several components of the Receptor Transporting Protein (RTP) family not present in the Ci8short mRNA. By means of Real Time PCR and Northern Blot, the Ci8short and Ci8long transcripts showed a different pattern of gene expression with the Ci8short mRNA being strongly activated after LPS injection in the pharynx. …

LipopolysaccharidesPolyadenylationCiona intestinaliSettore BIO/05 - Zoologialcsh:MedicineGene ExpressionBiochemistryGene expressionGene Orderlcsh:Science3' Untranslated RegionsPhylogenyIn Situ HybridizationRegulation of gene expressionMultidisciplinaryInnate ImmunityCiona intestinalisPhylogeneticsProtein TransportCytochemistryResearch ArticleDNA ComplementaryMolecular Sequence DataImmunologyIn situ hybridizationBiologyPolyadenylationModel OrganismsGeneticsAnimalsCiona intestinalisEvolutionary SystematicsNorthern blotAmino Acid SequenceRNA MessengerBiologyEvolutionary BiologyBase SequenceThree prime untranslated regionlcsh:RImmunityComputational BiologyProteinsImmune Defensebiology.organism_classificationMolecular biologyGenesinflammationSuppression subtractive hybridizationlcsh:Q5' Untranslated RegionsCiona intestinalis; inflammationSequence AlignmentPloS one
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CiC3-1a-Mediated Chemotaxis in the Deuterostome Invertebrate Ciona intestinalis (Urochordata)

2003

Abstract Deuterostome invertebrates possess complement genes, and in limited instances complement-mediated functions have been reported in these organisms. However, the organization of the complement pathway(s), as well as the functions exerted by the cloned gene products, are largely unknown. To address the issue of the presence of an inflammatory pathway in ascidians, we expressed in Escherichia coli the fragment of Ciona intestinalis C3-1 corresponding to mammalian complement C3a (rCiC3-1a) and assessed its chemotactic activity on C. intestinalis hemocytes. We found that the migration of C. intestinalis hemocytes toward rCiC3-1a was dose dependent, peaking at 500 nM, and was specific for…

Lipopolysaccharidescomplement system ascidiansHemocytesMolecular Sequence DataIn situ hybridizationPertussis toxinimmunologyHemolymphEscherichia coliAnimalsImmunology and AllergyCiona intestinalisAmino Acid SequencePeptide sequenceinnate immunityInflammationCell-Free SystemChemotactic FactorsbiologyImmune SeraRiboprobeChemotaxisAnatomybiology.organism_classificationRecombinant ProteinsComplement systemCell biologyCiona intestinalisChemotaxis LeukocyteHemocyte migrationPertussis ToxinCell Migration InhibitionComplement C3a
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Global Functional Analyses of Cellular Responses to Pore-Forming Toxins

2011

Here we present the first global functional analysis of cellular responses to pore-forming toxins (PFTs). PFTs are uniquely important bacterial virulence factors, comprising the single largest class of bacterial protein toxins and being important for the pathogenesis in humans of many Gram positive and Gram negative bacteria. Their mode of action is deceptively simple, poking holes in the plasma membrane of cells. The scattered studies to date of PFT-host cell interactions indicate a handful of genes are involved in cellular defenses to PFTs. How many genes are involved in cellular defenses against PFTs and how cellular defenses are coordinated are unknown. To address these questions, we pe…

MAPK/ERK pathwayTranscription GeneticImmunology/Innate ImmunityMessengerInteractomeInfectious Diseases/Bacterial InfectionsRNA interference2.1 Biological and endogenous factorsAetiologyBiology (General)Genes HelminthCaenorhabditis elegansOligonucleotide Array Sequence AnalysisGenetics0303 health sciencesGenomebiologyReverse Transcriptase Polymerase Chain ReactionGenetics and Genomics/Functional Genomics030302 biochemistry & molecular biologyrespiratory systemCell biologyInfectious DiseasesMedical MicrobiologyRNA InterferenceSignal transductionDNA microarrayTranscriptionBiotechnologyResearch ArticleSignal TransductionPore Forming Cytotoxic ProteinsQH301-705.5Virulence FactorsMAP Kinase Signaling System1.1 Normal biological development and functioningBacterial ToxinsImmunologyMicrobiologyDNA-binding proteinCell Line03 medical and health sciencesBacterial ProteinsGeneticUnderpinning researchVirologyEscherichia coliHelminthGeneticsAnimalsHumansRNA MessengerCaenorhabditis elegansCaenorhabditis elegans ProteinsMolecular BiologyGene030304 developmental biologyGenome HelminthCell MembraneGenetics and GenomicsRC581-607biology.organism_classificationrespiratory tract diseasesTranscription Factor AP-1Emerging Infectious DiseasesGenesRNAParasitologyGeneric health relevanceRNA HelminthImmunologic diseases. AllergyPLoS Pathogens
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Candida albicans Yeast and Hyphae are Discriminated by MAPK Signaling in Vaginal Epithelial Cells

2011

We previously reported that a bi-phasic innate immune MAPK response, constituting activation of the mitogen-activated protein kinase (MAPK) phosphatase MKP1 and c-Fos transcription factor, discriminates between the yeast and hyphal forms of Candida albicans in oral epithelial cells (ECs). Since the vast majority of mucosal Candida infections are vaginal, we sought to determine whether a similar bi-phasic MAPK-based immune response was activated by C. albicans in vaginal ECs. Here, we demonstrate that vaginal ECs orchestrate an innate response to C. albicans via NF-κB and MAPK signaling pathways. However, unlike in oral ECs, the first MAPK response, defined by c-Jun transcription factor acti…

MAPK/ERK pathwaylcsh:MedicineYeast and Fungal ModelsPathogenesisSignal transductionMolecular cell biologyCandida albicansGranulocyte Colony-Stimulating FactorCandida albicanslcsh:ScienceImmune Response0303 health sciencesMultidisciplinarybiologyCandidiasisNF-kappa BSignaling cascadesObstetrics and GynecologyCorpus albicansInnate ImmunityHost-Pathogen InteractionInfectious DiseasesVaginaCytokinesMedicineFemaleSignal transductionCandidalysinResearch ArticleMAPK signaling cascadesMAP Kinase Signaling SystemUrologyImmunologySexually Transmitted DiseasesHyphaeMycologyMicrobiologyMicrobiologyImmune Activation03 medical and health sciencesModel OrganismsHumansTranscription factorBiology030304 developmental biologyInnate immune systemChemokine CCL20030306 microbiologyGenitourinary InfectionsInterleukin-6lcsh:RImmunityFungiMouth MucosaImmune DefenseEpithelial Cellsbiology.organism_classificationImmunity InnateCCL20Immune Systemlcsh:QClinical ImmunologyPLoS ONE
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Cloning of Rac and Rho-GDI from tobacco using an heterologous two-hybrid screen.

2000

International audience; To examine whether molecular similarities exist between the animal and plant Rho GTPase signaling pathways, we have developed a heterologous two-hybrid screening method. By this technique, we have cloned a cDNA encoding a tobacco Rac-like protein able to interact with a mammalian Rho-GDI. In a second screen this tobacco Rac was used as a bait and a tobacco homologue of Rho-GDI was identified. These results show that some components of the animal and plant Rac signaling pathways are similar enough to allow their interaction in an heterologous approach. Moreover these data suggest a similar regulation of Rho GTPases in animals and plants.

MESH: Signal TransductionMESH: Plants ToxicMESH: Sequence Homology Amino Acid[SDV]Life Sciences [q-bio]Molecular Sequence DataMESH: rac GTP-Binding ProteinsMESH: Amino Acid SequenceMESH: Two-Hybrid System Techniques[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityMESH: Sequence AnalysisGene Expression Regulation PlantTwo-Hybrid System TechniquesTobacco[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansrho-Specific Guanine Nucleotide Dissociation InhibitorsMESH: Guanine Nucleotide Dissociation InhibitorsMESH: Cloning Molecular[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAmino Acid SequenceMESH: rho-Specific Guanine Nucleotide Dissociation InhibitorsCloning MolecularMESH: Gene Expression Regulation PlantMESH: Tobacco[SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunityComputingMilieux_MISCELLANEOUSGuanine Nucleotide Dissociation InhibitorsPlant ProteinsMESH: HumansMESH: Molecular Sequence DataSequence Homology Amino AcidMESH: Plant ProteinsGENETIQUErac GTP-Binding Proteins[SDV] Life Sciences [q-bio]Plants ToxicSequence AnalysisSignal Transduction
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Pathological significance and prognostic value of surfactant protein D in cancer

2018

Surfactant protein D (SP-D) is a pattern recognition molecule belonging to the Collectin (collagen-containing C-type lectin) family that has pulmonary as well as extra-pulmonary existence. In the lungs, it is a well-established opsonin that can agglutinate a range of microbes, and enhance their clearance via phagocytosis and super-oxidative burst. It can interfere with allergen–IgE interaction and suppress basophil and mast cell activation. However, it is now becoming evident that SP-D is likely to be an innate immune surveillance molecule against tumor development. SP-D has been shown to induce apoptosis in sensitized eosinophils derived from allergic patients and a leukemic cell line via …

Male0301 basic medicineLung NeoplasmsDatasets as Topic0302 clinical medicineEpidermal growth factorNeoplasmsImmunology and AllergyRNA NeoplasmOriginal ResearchCancerOvarian NeoplasmsInnate immunitySurfactant protein DBioinformatics analysiPrognosisPulmonary Surfactant-Associated Protein DImmunohistochemistryTumor microenvironment030220 oncology & carcinogenesisAdenocarcinomaFemaleCancersBreast NeoplasmHumanlcsh:Immunologic diseases. AllergyPrognosiImmunologyBreast NeoplasmsBiology03 medical and health sciencesImmune systemBioinformatics analysisStomach NeoplasmsStomach NeoplasmBiomarkers TumormedicineHumansComputer SimulationLung cancerTumor microenvironmentOvarian NeoplasmComputational BiologySurfactant protein DCancermedicine.diseaseSurvival AnalysisLung NeoplasmImmune surveillance030104 developmental biologyCancer researchNeoplasmBioinformatics analysis; Cancers; Immune surveillance; Immunohistochemistry; Innate immunity; Surfactant protein D; Tumor microenvironment; Immunology and Allergy; Immunologylcsh:RC581-607Ovarian cancer
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Association between the polymorphisms of TLR4 and CD14 genes and Alzheimer's disease.

2008

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. Inflammation plays a key role in AD and dissecting the genetics of inflammation may provide an answer to the possible treatment. Hence, the better understanding of different molecular and cellular inflammatory mechanisms is crucial for complete knowledge of AD pathophysiology, and for its prevention and drug therapy. Accordingly, in the present study we evaluated whether the pro-inflammatory polymorphisms of lipopolysaccaride-receptors, +896A/G Toll-Like Receptor (TLR4) and -260C/T CD14, are risk factors for AD. The study included both 626 AD …

MaleALZHEIMER'S DISEASEINFLAMMATIONINNATE IMMUNITYTLR4CD14Lipopolysaccharide ReceptorsInflammationSingle-nucleotide polymorphismDiseaseSystemic inflammationPolymorphism Single NucleotideSeverity of Illness IndexDegenerative diseaseINFLAMMATIONAlzheimer DiseaseRisk FactorsDrug DiscoverymedicineDementiaSNPHumansTLR4AgedPharmacologyAged 80 and overbusiness.industryMiddle Agedmedicine.diseaseToll-Like Receptor 4ItalyALZHEIMER'S DISEASEImmunologyINNATE IMMUNITYFemalemedicine.symptomAlzheimer's diseasebusinessCD14
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Increased Activity of Coagulation Factor XII (Hageman Factor) Causes Hereditary Angioedema Type III

2006

International audience; Hereditary angioedema (HAE) is characterized clinically by recurrent acute skin swelling, abdominal pain, and potentially life-threatening laryngeal edema. Three forms of HAE have been described. The classic forms, HAE types I and II, occur as a consequence of mutations in the C1-inhibitor gene. In contrast to HAE types I and II, HAE type III has been observed exclusively in women, where it appears to be correlated with conditions of high estrogen levels--for example, pregnancy or the use of oral contraceptives. A recent report proposed two missense mutations (c.1032C-->A and c.1032C-->G) in F12, the gene encoding human coagulation factor XII (FXII, or Hageman factor…

MaleTime FactorsKinins030204 cardiovascular system & hematologyMESH: Founder Effect[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityLinkage Disequilibrium0302 clinical medicineMissense mutationHereditary Angioedema Type IIIGenetics(clinical)MESH: Models GeneticGenetics (clinical)MESH: Heterozygote0303 health sciencesFactor XII[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyFounder EffectMarkov ChainsPedigree3. Good healthMESH: Linkage DisequilibriumFactor XIIHereditary angioedemaFemalemedicine.symptomMESH: Factor XIIHeterozygotemedicine.medical_specialtyMESH: MutationMESH: PedigreeMESH: Bayes TheoremCoagulation Factor XIIBiology03 medical and health sciencesMESH: Markov ChainsReportInternal medicinemedicineGeneticsHumansMESH: AngioedemaAngioedema030304 developmental biologyMESH: HumansModels GeneticAngioedemaHaplotypeMESH: Time FactorsBayes TheoremHeterozygote advantageMESH: Haplotypesmedicine.diseaseMESH: KininsMESH: MaleEndocrinologyHaplotypesMutationImmunologyMESH: Microsatellite RepeatsMESH: FemaleMicrosatellite RepeatsThe American Journal of Human Genetics
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Prognostic Value of Complement Properdin in Cancer

2021

© 2021 Mangogna, Varghese, Agostinis, Alrokayan, Khan, Stover, Belmonte, Martorana, Ricci, Bulla and Kishore. The complement system is readily triggered by the presence of damage-associated molecular patterns on the surface of tumour cells. The complement alternative pathway provides rapid amplification of the molecular stress signal, leading to complement cascade actvation to deal with pathogens or malignant cells. Properdin is the only known positive regulator of the alternative pathway. In addition, properdin promotes the phagocytic uptake of apoptotic T cells by macrophages and dendritic cells without activating the complement system, thus, establishing its ability to recognize “altered…

Malelcsh:Immunologic diseases. Allergybioinformatics analysisNeutrophilsComplement Pathway AlternativeImmunologyDatasets as TopicInflammationchemical and pharmacologic phenomenaBiologyLymphocytes Tumor-InfiltratingImmune systemNeoplasmsTumor Microenvironmentmedicinebioinformatics; cancer; complement; innate immunity; prognosis; properdinData MiningHumansImmunology and AllergyCytotoxic T cellcancercomplementRNA MessengerRNA Neoplasminnate immunityOriginal ResearchTumor microenvironmentInnate immune systembioinformaticMacrophagesDendritic CellsbioinformaticsLymphocyte SubsetsComplement systemproperdinAlternative complement pathwayCancer researchProperdinFemaleprognosismedicine.symptomTranscriptomelcsh:RC581-607prognostic markerprognosi
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