Search results for "PATHOGEN"

showing 10 items of 1657 documents

Immunohistochemistry of Human Hsp60 in Health and Disease: From Autoimmunity to Cancer

2017

Hsp60 (also called Cpn60) is a chaperonin with essential functions for cell physiology and survival. Additionally, its involvement in the pathogenesis of a variety of diseases (e.g., some autoimmune disorders and cancer) is becoming evident with new research. For example, the distribution and levels of Hsp60 in cells and tissues have been found altered in many pathologic conditions, and the significance of these alterations is being investigated in a number of laboratories. The aim of this ongoing research is to determine the meaning of these Hsp60 alterations with regard to pathogenetic mechanisms, diagnosis, classification of lesions, and assessing prognosis and response to treatment. Hsp…

0301 basic medicineCell physiologyHsp60 in cancerDiseasemedicine.disease_causeHsp60 immunostainingAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicineHsp60 and autoimmunityGeneticsmedicineMolecular BiologyHsp60 immunohistochemistrybusiness.industryCancerHsp60Hsp60 antibodiemedicine.diseaseChaperonin Hsp60Molecular mimicry030104 developmental biology030220 oncology & carcinogenesisImmunologyHsp60 locationImmunohistochemistryHSP60Hsp60 in tissuebusinessMolecular mimicry
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Epithelium‐specific MyD88 signaling, but not DCs or macrophages, control acute intestinal infection with Clostridium difficile

2019

Infection with Clostridium difficile is one of the major causes of health care acquired diarrhea and colitis. Signaling though MyD88 downstream of TLRs is critical for initiating the early protective host response in mouse models of C. difficile infection (CDI). In the intestine, MyD88 is expressed in various tissues and cell types, such as the intestinal epithelium and mononuclear phagocytes (MNP), including DC or macrophages. Using a genetic gain-of-function system, we demonstrate here that restricting functional MyD88 signaling to the intestinal epithelium, but also to MNPs is sufficient to protect mice during acute CDI by upregulation of the intestinal barrier function and recruitment o…

0301 basic medicineCell typeImmunologyBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationmedicineAnimalsImmunology and AllergyIntestinal MucosaColitisEnterocolitis PseudomembranousBarrier functionClostridioides difficileMacrophagesDendritic CellsClostridium difficilemedicine.diseaseIntestinal epitheliumPhenotypeEpitheliumDisease Models Animal030104 developmental biologymedicine.anatomical_structureHost-Pathogen InteractionsMyeloid Differentiation Factor 88ImmunologySignal Transduction030215 immunologyEuropean Journal of Immunology
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Autophagy in the pathogenesis of ankylosing spondylitis

2016

The pathogenesis of ankylosing spondylitis (AS) is not well understood, and treatment options have met with limited success. Autophagy is a highly conserved mechanism of controlled digestion of damaged organelles within a cell. It helps in the maintenance of cellular homeostasis. The process of autophagy requires the formation of an isolation membrane. They form double-membraned vesicles called “autophagosomes” that engulf a portion of the cytoplasm. Beyond the role in maintenance of cellular homeostasis, autophagy has been demonstrated as one of the most remarkable tools employed by the host cellular defense against bacteria invasion. Autophagy also affects the immune system and thus is im…

0301 basic medicineCellAutophagy-Related ProteinsATG16L1Cellular homeostasisInflammationBiologyLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Pathogenesis03 medical and health sciencesImmune systemRheumatologyATG16L1; Autophagy; Inflammation; LRRK2; Pathogenesis; Spondyloarthritis; RheumatologyPathogenesiAutophagymedicineHomeostasisHumansSpondylitis AnkylosingATG16L1InflammationAutophagyLRRK2General MedicineCell biology030104 developmental biologymedicine.anatomical_structureCytoplasmSpondyloarthritimedicine.symptomClinical Rheumatology
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Molecular Mechanism Involved in the Pathogenesis of Early-Onset Epileptic Encephalopathy

2019

Recent studies have shown that neurologic inflammation may both precipitate and sustain seizures, suggesting that inflammation may be involved not only in epileptogenesis but also in determining the drug-resistant profile. Extensive literature data during these last years have identified a number of inflammatory markers involved in these processes of “neuroimmunoinflammation” in epilepsy, with key roles for pro-inflammatory cytokines such as: IL-6, IL-17 and IL-17 Receptor (IL-17R) axis, Tumor-Necrosis-Factor Alpha (TNF-α) and Transforming-Growth-Factor Beta (TGF-β), all responsible for the induction of processes of blood-brain barrier (BBB) disruption and inflammation of the Central Nervou…

0301 basic medicineCentral nervous systemInflammationContext (language use)ReviewEpileptogenesisNOlcsh:RC321-571pathogenic mechanismsPathogenesis03 medical and health sciencesCellular and Molecular NeuroscienceEpilepsy0302 clinical medicineImmune systemMedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyPathologicalchildhoodbusiness.industrybiological markermedicine.diseaseepileptic encephalopathy030104 developmental biologymedicine.anatomical_structureinflammationmedicine.symptombusinessNeurosciencebiological markers030217 neurology & neurosurgeryNeurosciencebiological markers epileptic encephalopathy inflammation pathogenic mechanisms childhoodFrontiers in Molecular Neuroscience
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COVID-19: viral–host interactome analyzed by network based-approach model to study pathogenesis of SARS-CoV-2 infection

2020

AbstractBackgroundEpidemiological, virological and pathogenetic characteristics of SARS-CoV-2 infection are under evaluation. A better understanding of the pathophysiology associated with COVID-19 is crucial to improve treatment modalities and to develop effective prevention strategies. Transcriptomic and proteomic data on the host response against SARS-CoV-2 still have anecdotic character; currently available data from other coronavirus infections are therefore a key source of information.MethodsWe investigated selected molecular aspects of three human coronavirus (HCoV) infections, namely SARS-CoV, MERS-CoV and HCoV-229E, through a network based-approach. A functional analysis of HCoV-hos…

0301 basic medicineChemokinevirusesPneumonia ViralGene regulatory networklcsh:MedicineComputational biologyVirus-host interactomemedicine.disease_causeModels BiologicalInteractomeGeneral Biochemistry Genetics and Molecular BiologyTranscriptomePathogenesis03 medical and health sciencesBetacoronavirus0302 clinical medicineViral Envelope ProteinsProtein Interaction MappingmedicineCoronavirus infectionHumansGene Regulatory NetworksPandemicsGeneCoronavirusVirus–host interactomeMembrane GlycoproteinsInnate immune systembiologySARS-CoV-2Researchlcsh:RCOVID-19virus diseasesGeneral Medicinebiochemical phenomena metabolism and nutritionVirus–host interactome ; COVID-19 ; Coronavirus infection ; Spike glycoproteinPhenotyperespiratory tract diseasescoronavirus infection; spike glycoprotein; virus-host interactome030104 developmental biologySettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICA030220 oncology & carcinogenesisHost-Pathogen Interactionsbiology.proteinSpike glycoproteinCoronavirus InfectionsSignal TransductionJournal of Translational Medicine
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INFLAMMATORY BOWEL DISEASE, COLORECTAL CANCER AND TYPE 2 DIABETES MELLITUS: THE LINKS

2016

The co-occurrence of the three disease entities, inflammatory bowel disease (IBD), colorectal cancer (CRC), type 2diabetes mellitus (T2DM) along with inflammation and dismicrobism has been frequently reported. Some authors have even suggested that dysbiosis could be the link through a molecular crosstalk of multiple inflammatory loops including TGFβ, NFKB, TNFα and ROS among others. This review focuses on the inflammatory process along with the role of microbiota in the pathophysiology of the three diseases. The etiology of IBD is multifactorial, and like CRC and T2DM, it is associated with a widespread and sustained GI inflammation and dismicrobism, whereby an array of pro-inflammatory med…

0301 basic medicineColorectal cancerIBDT2DMInflammationDiseaseReviewSystemic inflammationProbioticInflammatory bowel diseasePathology and Forensic MedicinePathogenesis03 medical and health sciences0302 clinical medicinePhysiology (medical)medicineInflammationbusiness.industrymedicine.diseasedigestive system diseasesCRC030104 developmental biology030220 oncology & carcinogenesisImmunologyInflammatory Bowel diseases IBD colorectal cancer diabetes mellitusMolecular MedicineDysbiosisTumor necrosis factor alphamedicine.symptombusinessDysbiosis
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Hsp60 as a Novel Target in IBD Management: A Prospect

2019

Inflammatory bowel disease (IBD) encompasses various pathological conditions similar but distinct that share a multifactorial etiology, including involvement of the intestinal barrier function, the immune system, and intestinal microorganisms. Hsp60 is a chaperonin component of the chaperoning system, present in all cells and tissues, including the intestine. It plays important roles in cell physiology outside and inside mitochondria, its canonical place of residence. However, Hsp60 can also be pathogenic in many conditions, the Hsp60 chaperonopathies, possibly including IBD. The various clinico-pathological types of IBD have a complicated mix of causative factors, among which Hsp60 can be …

0301 basic medicineColorectal cancerMini Reviewchaperoning systemDiseaseBioinformaticsInflammatory bowel diseasePathogenesis03 medical and health sciences0302 clinical medicineImmune systemintestinal wallinflammatory bowel diseasemedicinemicrobiotaPharmacology (medical)PathologicalchaperonotherapyPharmacologybusiness.industrylcsh:RM1-950fungimedicine.diseaseHsp60Biomarkerimmune systemlcsh:Therapeutics. Pharmacology030104 developmental biology030220 oncology & carcinogenesisEtiologychaperonopathybusinessFrontiers in Pharmacology
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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
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Succinate Activates EMT in Intestinal Epithelial Cells through SUCNR1: A Novel Protagonist in Fistula Development

2020

The pathogenesis of Crohn&rsquo

0301 basic medicineCrohn’s diseaseFistulaSuccinic Acid610 Medicine & healthVimentinArticleReceptors G-Protein-CoupledPathogenesis03 medical and health sciencesHT29 Cells0302 clinical medicineCrohn DiseaseFibrosismedicineGene silencingAnimalsHumansfistulaReceptorlcsh:QH301-705.5InflammationbiologyChemistryMesenchymal stem cellWnt signaling pathwayEpithelial CellsGeneral Medicinemedicine.diseaseCadherinssuccinateFibrosisdigestive system diseasesIntestinesCrohn's disease10219 Clinic for Gastroenterology and Hepatology030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisbiology.proteinCancer research
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STAT1 Isoforms Differentially Regulate NK Cell Maturation and Anti-tumor Activity

2020

Natural killer (NK) cells are important components of the innate immune defense against infections and cancers. Signal transducer and activator of transcription 1 (STAT1) is a transcription factor that is essential for NK cell maturation and NK cell-dependent tumor surveillance. Two alternatively spliced isoforms of STAT1 exist: a full-length STAT1α and a C-terminally truncated STAT1β isoform. Aberrant splicing is frequently observed in cancer cells and several anti-cancer drugs interfere with the cellular splicing machinery. To investigate whether NK cell-mediated tumor surveillance is affected by a switch in STAT1 splicing, we made use of knock-in mice expressing either only the STAT1α (S…

0301 basic medicineCytotoxicity ImmunologicLymphomaNK cellsCell MaturationMice0302 clinical medicineInterferonImmunology and AllergyProtein IsoformsSTAT1Immunologic SurveillanceOriginal ResearchBone Marrow TransplantationReceptors InterferonInterleukin-15Mice KnockoutLymphopoiesisinterferonInterferon-Stimulated Gene Factor 3Cell biologySpecific Pathogen-Free OrganismsKiller Cells NaturalSTAT1 Transcription FactorOrgan SpecificityMHC class ISignal transductionsignal transductionmedicine.druglcsh:Immunologic diseases. AllergyLymphoid TissueImmunologyBiologyLymphocyte Depletion03 medical and health sciencesInterleukin-15 Receptor alpha SubunitCell Line TumormedicineAnimalsTranscription factorInnate immune systemisoformsMice Inbred C57BL030104 developmental biologyCancer cellSTAT proteinbiology.proteinlcsh:RC581-607IL-15RαSpleen030215 immunologyFrontiers in Immunology
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