Search results for "inflammation."

showing 10 items of 2627 documents

Cell-Type-Specific Responses to Interleukin-1 Control Microbial Invasion and Tumor-Elicited Inflammation in Colorectal Cancer.

2017

Summary Chronic inflammation drives the progression of colorectal cancer (CRC). Increased expression of interleukin (IL)-17A is associated with poor prognosis, and IL-17A blockade curbs tumor progression in preclinical models of CRC. Here we examined the impact of IL-1 signaling, a key regulator of the IL-17 pathway, in different cell types within the CRC microenvironment. Genetic deletion of the IL-1 receptor (IL-1R1) in epithelial cells alleviated tumorigenesis in the APC model of CRC, demonstrating a cell-autonomous role for IL-1 signaling in early tumor seed outgrowth. T cell specific ablation of IL-1R1 decreased tumor-elicited inflammation dependent on IL-17 and IL-22, thereby reducing…

0301 basic medicineCell typeColorectal cancerCarcinogenesisNeutrophilsmedicine.medical_treatmentImmunologyMedizinInflammationBiologymedicine.disease_causeArticle03 medical and health sciencesMice0302 clinical medicineSalmonellamedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumansCells CulturedInflammationMice KnockoutTumor microenvironmentSalmonella Infections AnimalInterleukinsInterleukin-17InterleukinReceptors Interleukin-1medicine.disease030104 developmental biologyInfectious DiseasesCytokineTumor progressionOrgan Specificity030220 oncology & carcinogenesisCancer researchmedicine.symptomCarcinogenesisColorectal NeoplasmsInterleukin-1Signal TransductionImmunity
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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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Tnfaip3 expression in pulmonary conventional type 1 Langerin‐expressing dendritic cells regulates T helper 2‐mediated airway inflammation in mice

2020

Abstract Background Conventional type 1 dendritic cells (cDC1s) control anti‐viral and anti‐tumor immunity by inducing antigen‐specific cytotoxic CD8+ T‐cell responses. Controversy exists whether cDC1s also control CD4+ T helper 2 (Th2) cell responses, since suppressive and activating roles have been reported. DC activation status, controlled by the transcription factor NF‐κB, might determine the precise outcome of Th‐cell differentiation upon encounter with cDC1s. To investigate the role of activated cDC1s in Th2‐driven immune responses, pulmonary cDC1s were activated by targeted deletion of A20/Tnfaip3, a negative regulator of NF‐κB signaling. Methods To target pulmonary cDC1s, Cd207 (Lan…

0301 basic medicineCellDUSTCD8-Positive T-LymphocytesINHALED ANTIGENTh2&#8208Mice0302 clinical medicineTnfaip3Medicine and Health SciencesCytotoxic T cellImmunology and AllergyInterferon gammaLungSensitizationMice KnockoutCONSTITUTIVE EXPRESSIONIFN-GAMMAbiologyCD8(+) T cellsType 1 conventional dendritic cellsIMMUNE-RESPONSES3. Good healthmedicine.anatomical_structureA20Original Articlemedicine.drugLangerinImmunologyCD8+ T cells03 medical and health sciencesImmune systemTh2 CellsImmunitymedicineAnimalsdriven airway inflammationCD103(+)InflammationBiology and Life SciencesTH2 RESPONSESA20/Tnfaip3Dendritic CellsTh2‐driven airway inflammationMice Inbred C57BL030104 developmental biologyinterferon gamma030228 respiratory systemImmunologybiology.proteinASTHMABasic and Translational Allergy ImmunologyORIGINAL ARTICLESCD8LUNGAllergy
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Tc17 biology and function: Novel concepts

2020

Research over the past years has provided increasing understanding about IL-17-producing CD8+ T cells termed Tc17 or IL-17+ CD8+ T cells, their distribution and role in a range of diverse immune processes. These comprise resistance to pathogens and tissue homeostasis, but also contribution to autoimmunity and cancer, as well as involvement in gut inflammation, lung diseases and graft-versus-host-disease. Tc17 cells are regulated by unique differentiation mechanisms distinguishing them from other IL-17-producing T cells, including Th17, mucosal-associated invariant T cells, and γδ17 T cells, thus ensuring their specific function in immune responses. Here, we review recent advances in underst…

0301 basic medicineCellular differentiationInterleukin-17ImmunologyInflammationCD8-Positive T-LymphocytesBiologymedicine.disease_causeAutoimmunity03 medical and health sciences030104 developmental biology0302 clinical medicineImmune systemT-Lymphocyte SubsetsImmunologymedicineAnimalsHumansImmunology and AllergyCytotoxic T cellInterleukin 17medicine.symptomCD8Tissue homeostasis030215 immunologyEuropean Journal of Immunology
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Bifidobacterium CECT 7765 modulates early stress-induced immune, neuroendocrine and behavioral alterations in mice.

2016

Emerging evidence suggests that there is a window of opportunity within the early developmental period, when microbiota-based interventions could play a major role in modulating the gut-brain axis and, thereby, in preventing mood disorders. This study aims at evaluating the effects and mode of action of Bifidobacterium pseudocatenulatum CECT 7765 in a murine model of chronic stress induced by maternal separation (MS). C57Bl/6J male breast-fed pups were divided into four groups, which were subjected or not to MS and supplemented with placebo or B. pseudocatenulatum CECT7765 until postnatal period (P) 21 and followed-up until P41. Behavioral tests were performed and neuroendocrine parameters …

0301 basic medicineCentral Nervous SystemMalemedicine.medical_specialtyHypothalamo-Hypophyseal Systemmedicine.medical_treatmentImmunologyBifidobacterium pseudocatenulatumPituitary-Adrenal SystemInflammationBiologyDiet High-Fat03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineImmune systemCorticosteroneStress PhysiologicalInternal medicineRNA Ribosomal 16SmedicineAnimalsChronic stressObesityNeurotransmitterInflammationNeurotransmitter AgentsEndocrine and Autonomic SystemsMaternal DeprivationMicrobiotaProbioticsNeurosecretory SystemsIntestinesMice Inbred C57BL030104 developmental biologyCytokineEndocrinologychemistryHypothalamusImmunologyDietary SupplementsCytokinesBifidobacteriummedicine.symptom030217 neurology & neurosurgeryBrain, behavior, and immunity
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Gut-CNS-Axis as Possibility to Modulate Inflammatory Disease Activity-Implications for Multiple Sclerosis.

2017

In the last decade the role of environmental factors as modulators of disease activity and progression has received increasing attention. In contrast to classical environmental modulators such as exposure to sun-light or fine dust pollution, nutrition is an ideal tool for a personalized human intervention. Various studies demonstrate a key role of dietary factors in autoimmune diseases including Inflammatory Bowel Disease (IBD), rheumatoid arthritis or inflammatory central nervous system (CNS) diseases such as Multiple Sclerosis (MS). In this review we discuss the connection between diet and inflammatory processes via the gut–CNS-axis. This axis describes a bi-directional communication syst…

0301 basic medicineCentral Nervous SystemMultiple SclerosisCentral nervous systemInflammationReviewBiologyInflammatory bowel diseaseModels BiologicalCatalysisInorganic ChemistryDisease activitylcsh:Chemistry03 medical and health sciencesImmune systemmedicinemicrobiotaAnimalsHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyInflammationMultiple sclerosisOrganic ChemistryGeneral Medicinemedicine.diseaseComputer Science ApplicationsGastrointestinal Tractgut–CNS-axisimmune system030104 developmental biologymedicine.anatomical_structurenutritionlcsh:Biology (General)lcsh:QD1-999Rheumatoid arthritisAdjunctive treatmentImmunologymedicine.symptomInternational journal of molecular sciences
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CNS-localized myeloid cells capture living invading T cells during neuroinflammation

2020

Using an in vivo real-time approach, the authors show that local myeloid cells remove early CNS-invading T cells via an engulfment pathway that is dependent on N-acetyl-D-glucosamine (GlcNAc) and lectin. These results reveal a novel capacity of myeloid cells to counteract neuroinflammation.

0301 basic medicineCentral Nervous SystemProgrammed cell deathCell signalingEncephalomyelitis Autoimmune ExperimentalCell SurvivalEncephalomyelitisT cellT-LymphocytesImmunologyInnate Immunity and InflammationCX3C Chemokine Receptor 1AutoimmunityReceptors Cell SurfaceCell CommunicationPhosphatidylserinesBiologyLymphocyte ActivationSeverity of Illness IndexArticle03 medical and health sciencesMice0302 clinical medicineNeuroinflammationPhagocytosisIn vivomedicineImmunology and AllergyAnimalsLectins C-TypeMyeloid CellsNeuroinflammationInflammationGlucosamineCell DeathExperimental autoimmune encephalomyelitismedicine.diseaseCell biology030104 developmental biologymedicine.anatomical_structureMannose-Binding LectinsTh17 Cells030217 neurology & neurosurgeryEx vivoMannose ReceptorThe Journal of Experimental Medicine
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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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Overview of General and Discriminating Markers of Differential Microglia Phenotypes.

2020

Inflammatory processes and microglia activation accompany most of the pathophysiological diseases in the central nervous system. It is proven that glial pathology precedes and even drives the development of multiple neurodegenerative conditions. A growing number of studies point out the importance of microglia in brain development as well as in physiological functioning. These resident brain immune cells are divergent from the peripherally infiltrated macrophages, but their precise in situ discrimination is surprisingly difficult. Microglial heterogeneity in the brain is especially visible in their morphology and cell density in particular brain structures but also in the expression of cell…

0301 basic medicineCentral nervous systemInflammationReviewBiologylcsh:RC321-571M1/M2 phenotype03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineImmune systemneurotoxicitymedicineCytotoxic T celllcsh:Neurosciences. Biological psychiatry. NeuropsychiatrypolarizationMicrogliaRegeneration (biology)Neurotoxicityinfiltrating macrophagesmedicine.diseasePhenotype030104 developmental biologymedicine.anatomical_structureinflammationCellular Neuroscienceregenerationmicroglial heterogeneitymedicine.symptomNeuroscience030217 neurology & neurosurgeryFrontiers in cellular neuroscience
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Angiotensin II and leukocyte trafficking: New insights for an old vascular mediator. Role of redox-signaling pathways.

2019

Abstract Inflammation and activation of the immune system are key molecular and cellular events in the pathogenesis of cardiovascular diseases, including atherosclerosis, hypertension-induced target-organ damage, and abdominal aortic aneurysm. Angiotensin II (Ang-II) is the main effector peptide hormone of the renin-angiotensin system. Beyond its role as a potent vasoconstrictor and regulator of blood pressure and fluid homeostasis, Ang-II is intimately involved in the development of vascular lesions in cardiovascular diseases through the activation of different immune cells. The migration of leukocytes from circulation to the arterial subendothelial space is a crucial immune response in le…

0301 basic medicineChemokineEndotheliumInflammationBiochemistry03 medical and health sciences0302 clinical medicineMediatorImmune systemPhysiology (medical)Leukocyte TraffickingLeukocytesMedicinebiologybusiness.industryCell adhesion moleculeAngiotensin IIEndothelial CellsAngiotensin IICell biology030104 developmental biologymedicine.anatomical_structurebiology.proteinmedicine.symptombusinessOxidation-Reduction030217 neurology & neurosurgerySignal TransductionFree radical biologymedicine
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