Search results for "inflammation"

showing 10 items of 2662 documents

Lung-restricted activation of the alveolar macrophage/monocyte system in pulmonary sarcoidosis.

1992

An activation of T-cells that is restricted to the lung has been demonstrated in pulmonary sarcoidosis. The role of blood monocytes (MO) and alveolar macrophages (AM) in this concept of compartmentalized inflammation has not yet been evaluated. In order to elucidate this question, we measured the release of tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1) by peripheral blood mononuclear cells (PBMNC) and AM in 43 patients with sarcoidosis (32 with active, 11 with inactive disease) without therapy and correlated the spontaneous monokine release to parameters of the T-cell alveolitis and the course of the disease. TNF alpha as well as IL-1 were spontaneously released by AM of …

Pulmonary and Respiratory MedicineInterleukin 2Lung Diseasesmedicine.medical_specialtyTime FactorsSarcoidosisLung Diseases/metabolism610 MedizinInflammationSarcoidosis/metabolismLymphocyte ActivationMacrophages Alveolar/secretionPeripheral blood mononuclear cellMonocytesInterleukin-1/secretionInternal medicineMacrophages AlveolarmedicineMacrophageHumansddc:610Receptors Interleukin-2/metabolismTumor Necrosis Factor-alpha/secretionbusiness.industryTumor Necrosis Factor-alphaMonocyteLeukocytes Mononuclear/secretionMonocytes/immunologyReceptors Interleukin-2Macrophage ActivationMonokinemedicine.anatomical_structureEndocrinologyImmunologyAlveolar macrophageLeukocytes MononuclearInterleukin-2Tumor necrosis factor alphamedicine.symptomInterleukin-2/secretionbusinessmedicine.drugInterleukin-1The American review of respiratory disease
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Modulation of endotoxin-induced neutrophil transendothelial migration by alveolar epithelium in a defined bilayer model.

2006

Within the alveolus, epithelial cells, due to their close association with endothelial cells, can potentially influence endothelial cell responsiveness during inflammation and their interaction with leukocytes. To investigate this, three lung epithelial cell lines (A549, Calu-3, or NCI-H441) were grown with endothelium on opposing surfaces of Transwell filters and the formation and stability of bilayers was rigorously evaluated. All epithelial lines disrupted endothelial monolayer formation on filters with 3- or 5-microm pores by breaching the filter, and this occurred regardless of seeding density, matrix composition, or duration of culture. Endothelial disruption was not detectable by ele…

Pulmonary and Respiratory MedicineLipopolysaccharidesEndotheliumNeutrophilsClinical BiochemistryInflammationEnzyme-Linked Immunosorbent AssayBiologyUmbilical veinCell LineCell MovementmedicineHumansMolecular BiologyA549 cellLung alveolusMicropore FiltersEpitheliumCoculture TechniquesCell biologyEndothelial stem cellPulmonary Alveolimedicine.anatomical_structureCell cultureImmunologyEndothelium Vascularmedicine.symptomExperimental lung research
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The Non-neuronal cholinergic system: an emerging drug target in the airways.

2001

The non-neuronal cholinergic system is widely expressed in human airways. Choline acetyltransferase (ChAT) and/or acetylcholine are demonstrated in more or less all epithelial surface cells (goblet cells, ciliated cells, basal cells), submucosal glands and airway smooth muscle fibres. Acetylcholine is also demonstrated in the effector cells of the immune system (lymphocytes, macrophages, mast cells). Epithelial, endothelial and immune cells express nicotinic and muscarinic receptors. Thus the cytomolecule acetylcholine can contribute to the regulation of basic cell functions via auto-/paracrine mechanisms (proliferation, differentiation, ciliary activity, secretion of water, ions and mucus,…

Pulmonary and Respiratory MedicineLung Diseasesmedicine.medical_specialtyInflammationBiologyReceptors NicotinicCholine O-AcetyltransferaseImmune systemInternal medicineMuscarinic acetylcholine receptorMuscarinic acetylcholine receptor M5medicineHomeostasisHumansPharmacology (medical)InflammationImmunity CellularBiochemistry (medical)Muscarinic acetylcholine receptor M3Epithelial CellsMuscle SmoothCholine acetyltransferaseReceptors MuscarinicAcetylcholineCell biologyNicotinic agonistEndocrinologyAntibody Formationmedicine.symptomAcetylcholinemedicine.drugPulmonary pharmacologytherapeutics
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Obstructive sleep apnoea in acute coronary syndrome.

2019

Obstructive sleep apnoea (OSA) syndrome affects about 13% of the male and 7–9% of the female population. Hypoxia, oxidative stress and systemic inflammation link OSA and cardiovascular and metabolic consequences, including coronary artery disease. Current research has identified several clinical phenotypes, and the combination of breathing disturbances during sleep, systemic effects and end-organ damage might help to develop personalised therapeutic approaches. It is unclear whether OSA is a risk factor for acute coronary syndrome (ACS) and might affect its outcome. On the one hand, OSA in patients with ACS may worsen prognosis; on the other hand, OSA-related hypoxaemia could favour the dev…

Pulmonary and Respiratory MedicineMaleAcute coronary syndromemedicine.medical_specialtymedicine.medical_treatmentSettore MED/10 - Malattie Dell'Apparato Respiratorio030204 cardiovascular system & hematologySystemic inflammationCoronary artery disease03 medical and health sciences0302 clinical medicineRisk FactorsInternal medicinePositive airway pressurePrevalenceMedicineHumansContinuous positive airway pressureNon disponibiliAcute Coronary SyndromeAdverse effectLunglcsh:RC705-779Sleep Apnea ObstructiveContinuous Positive Airway Pressurebusiness.industryRespirationHemodynamicsSleep apnealcsh:Diseases of the respiratory systemHypoxia (medical)medicine.diseasenervous system diseasesrespiratory tract diseasesTreatment Outcome030228 respiratory systemCardiologyPatient ComplianceFemalemedicine.symptombusinessSleepEuropean respiratory review : an official journal of the European Respiratory Society
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Neutrophil activation in severe, early-onset COPD patients versus healthy non-smoker subjects in vitro: effects of antioxidant therapy.

2011

<i>Background:</i> Neutrophils and oxidative stress have been implicated in the pathogenesis of COPD. Severe, early-onset COPD is characterized by a rapid decline in the lung function at an early age; however, nothing is known about neutrophil activation in COPD patients. <i>Objectives:</i> The aim of this study was to evaluate peripheral blood neutrophil activation in severe, early-onset COPD patients versus healthy non-smokers and the effect of N-acetyl-<i>L</i>-cysteine (NAC) on neutrophil activation in vitro. <i>Methods:</i> Neutrophils were isolated from 15 severe, early-onset COPD patients and 15 age-matched healthy subjects and stimulat…

Pulmonary and Respiratory MedicineMaleAntioxidantCopd patientsNeutrophilsmedicine.medical_treatmentInflammationApoptosismacromolecular substancesmedicine.disease_causeNeutrophil ActivationPathogenesisPulmonary Disease Chronic ObstructivemedicineHumansSulfhydryl CompoundsEarly onsetCOPDbusiness.industryChemotaxisInterleukin-8Free Radical ScavengersMiddle Agedmedicine.diseaseIn vitrorespiratory tract diseasesAcetylcysteineN-Formylmethionine Leucyl-PhenylalanineCase-Control StudiesImmunologyFemalemedicine.symptombusinessLeukocyte ElastaseReactive Oxygen SpeciesOxidative stressRespiration; international review of thoracic diseases
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Endurance training damages small airway epithelium in mice.

2007

RATIONALE: In athletes, airway inflammatory cells were found to be increased in induced sputum or bronchial biopsies. Most data were obtained after exposure to cold and dry air at rest or during exercise. Whether training affects epithelial and inflammatory cells in small airways is unknown. OBJECTIVES: To test whether endurance training under standard environmental conditions causes epithelial damage and inflammation in the small airways of mice. METHODS AND MEASUREMENTS: Formalin-fixed, paraffin-embedded lung sections were obtained in sedentary (n = 14) and endurance-trained (n = 16) Swiss mice at baseline and after 15, 30, and 45 days of training. The following variables were assessed (m…

Pulmonary and Respiratory MedicineMalePathologymedicine.medical_specialtyInflammationApoptosisCritical Care and Intensive Care MedicineSettore BIO/09 - FisiologiaEpitheliumEpithelial DamageLeukocyte CountMiceEndurance trainingIntensive carePhysical Conditioning AnimalProliferating Cell Nuclear AntigenmedicineLeukocytesAnimalsBronchitisCell ProliferationBasement membraneLungAerobic exercise bronchial responsivenes methacholine deep inspiration leukotrienesbusiness.industryNF-kappa Brespiratory systemImmunohistochemistryEpitheliumrespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureRespiratory epitheliummedicine.symptombusinessAmerican journal of respiratory and critical care medicine
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Reduced apoptosis of CD8+ T-Lymphocytes in the airways of smokers with mild/moderate COPD

2011

SummaryChronic obstructive pulmonary disease (COPD) is characterised by chronic inflammation in airways and lung parenchyma. CD8+ T-lymphocytes, crucial effector and regulatory cells in inflammation, are increased in the central and peripheral airways in COPD. The aim of this study was to assess the role of apoptosis in the accumulation of CD8+ T-lymphocytes within the airway wall in COPD. We examined the submucosa of transverse sections of central and peripheral airways from post-operative tissues from non-smokers (n = 16), smokers with normal lung function (n = 16), smokers with mild/moderate COPD (n = 16), and smokers with severe/very severe COPD (n = 9). TUNEL and immunohistochemistry t…

Pulmonary and Respiratory MedicineMaleapoptosis cytotoxic T-lymphocytes inflammation lung tissueInflammationApoptosisSettore MED/10 - Malattie Dell'Apparato RespiratorioCD8-Positive T-LymphocytesFEV1/FVC ratioPulmonary Disease Chronic ObstructiveSubmucosaForced Expiratory VolumeParenchymamedicineHumansLungLung tissueInflammationCOPDAnalysis of VarianceLungbusiness.industryCytotoxic T-lymphocytesSmokingMiddle Agedrespiratory systemmedicine.diseaseImmunohistochemistryrespiratory tract diseasesmedicine.anatomical_structureImmunologybehavior and behavior mechanismsFemalemedicine.symptomAirwaybusinessCD8Respiratory Medicine
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Retroaortic left renal vein and inflammatory abdominal aortic aneurysm

2010

The aim of this study was to report successful surgical management of an inflammatory abdominal aortic aneurysm associated with a retroaortic left renal vein. The patient, a 78-year-old man, presented with diffuse abdominal pain, fever, and constipation. Contrast-enhanced computed tomography showed soft tissue surrounding the aneurysm and a left renal vein behind the aorta. Intraoperative findings confirmed the CT images. The patient is alive and well 6 months postoperatively.

Pulmonary and Respiratory MedicineMalemedicine.medical_specialtyAbdominal painFeverAortographySettore MED/22 - Chirurgia VascolareRenal VeinsAortic aneurysmBlood Vessel Prosthesis ImplantationAneurysmmedicine.arteryMedicineHumansAgedInflammationAortabusiness.industrySoft tissueGeneral Medicinemedicine.diseaseCardiac surgeryAbdominal PainTreatment OutcomeCardiothoracic surgerycardiovascular systemInflammatory abdominal aortic aneurysm Retroaortic left renal vein Open repairSurgeryRadiologymedicine.symptomCardiology and Cardiovascular MedicinebusinessTomography X-Ray ComputedConstipationAbdominal surgeryAortic Aneurysm Abdominal
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Oral N-acetylcysteine attenuates the rat pulmonary inflammatory response to antigen.

2003

Oxidative stress is involved in the pathophysiology of inflammatory airway diseases including asthma; therefore, antioxidants might be of clinical benefit in asthma treatment. In the present study, the effects of N-acetylcysteine on sensitised brown Norway rats were examined. N-Acetylcysteine (3 mmol kg body weight(-1) administered orally) was given daily for 1 week before challenge and various antigen-induced pulmonary responses were studied. Antigen exposure increased lipid peroxidation in bronchoalveolar lavage fluid (BALF) and oxidised glutathione levels in lung tissue 2 h after challenge. Lung nuclear transcription factor-KB-binding activity was increased 2 h after challenge, and BALF …

Pulmonary and Respiratory MedicineMalemedicine.medical_treatmentMolecular Sequence DataAdministration OralNitric Oxide Synthase Type IIInflammationPharmacologyBronchial Provocation TestsAcetylcysteinechemistry.chemical_compoundMedicineAnimalsEvans BlueProbabilityAnalysis of VarianceLungmedicine.diagnostic_testBase Sequencebusiness.industryReverse Transcriptase Polymerase Chain ReactionAirway Resistancerespiratory systemEosinophilAllergensIntercellular Adhesion Molecule-1ExtravasationAsthmarespiratory tract diseasesAcetylcysteineRatsDisease Models AnimalCytokinemedicine.anatomical_structureBronchoalveolar lavagechemistryImmunologyLipid Peroxidationmedicine.symptomBronchial HyperreactivityInflammation MediatorsNitric Oxide SynthasebusinessBronchoalveolar Lavage Fluidmedicine.drugThe European respiratory journal
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Airway remodeling in asthma.

2003

Chronic inflammation and remodeling may follow acute inflammation or may begin insidiously as a low-grade smoldering response, especially in the case of immune reactions. The histologic hallmarks of chronic inflammation and remodeling are as follows: (1) infiltration by macrophages and lymphocytes; (2) proliferation of fibroblasts that may take the form of myofibroblasts; (3) angiogenesis; (4) increased connective tissue (fibrosis); and (5) tissue destruction. It is clear that changes in the extracellular matrix, smooth muscle, and mucous glands have the capacity to influence airway function and reactivity in asthma patients. However, it is not known how each of the many structural changes …

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtyWound Healingbusiness.industryRespiratory diseaseRespiratory SystemInflammationrespiratory systemAirway obstructionCritical Care and Intensive Care Medicinemedicine.diseaseAsthmarespiratory tract diseasesBronchial hyperresponsivenessFibrosisImmunologymedicineHumansmedicine.symptomCardiology and Cardiovascular MedicinebusinessAirwayMyofibroblastAsthmaChest
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