Similar levels of nitric oxide in exhaled air in non-asthmatic rhinitis and asthma after bronchial allergen challenge
| Autor: | Julia G. Koopmans, Christa E. Lopuhaä, J. S. Van Der Zee, Henk M. Jansen |
|---|---|
| Přispěvatelé: | Pulmonology |
| Jazyk: | angličtina |
| Rok vydání: | 2003 |
| Předmět: |
Adult
Male Allergy Rhinitis Allergic Perennial Time Factors Immunology Provocation test medicine.disease_cause Nitric Oxide Bronchial Provocation Tests Nitric oxide chemistry.chemical_compound Allergen immune system diseases Forced Expiratory Volume Administration Inhalation medicine Immunology and Allergy Humans Expiration Prospective Studies Asthma Inhalation business.industry Respiratory disease Pyroglyphidae Allergens medicine.disease Bronchodilator Agents respiratory tract diseases chemistry Female business Histamine |
| Zdroj: | Allergy, 58(4), 300-305. Wiley-Blackwell |
| ISSN: | 0105-4538 |
| Popis: | Nitricoxideinexhaledair(eNO)iselevatedinasthma(1)andtoalesserextentinnon-asthmaticrhinitisaswell(2,3). Measuring eNO has been proposed as a diagnostictoolforasthma(1),bothinadultsandinchildren(4).Inaddition, eNO is advocated to be a valuable mean ofmonitoring asthmatic patients (5), as eNO seems to berelated to the degree of bronchial inflammation inasthma. On the one hand eNO decreases during treat-ment with inhaled steroids (6) and on the other eNOincreasesafterallergenchallenge(7).ApartfromthepotentialclinicalusefulnessofeNOinasthma,nitricoxide(NO)isaninterestingmoleculeinthepathophysiology of asthma and rhinitis because of itspossibleimmunologiceffects.Allergicdiseasesaregener-allyassumedtobecharacterizedbyashiftinthebalancebetweenTh1andTh2cellstowardTh2cells.Nitricoxidecauses prolonged suppression of Interferon (IFN)-cproduction byhelper T (Th) cellsinvitro(8). As IFNcis one of the key cytokines in the differentiation of ThcellsintoTh1andTh2subsetsandinhibitstheprolifer-ationoftheTh2cells,NOmightindirectlyenhancetheTh2-mediated inflammatory response in allergic asthmaandallergicrhinitisbythesuppressionofIFN-c.TheincreasedlevelofeNOisconsideredtobecausedbyupregulationoftheinducibleformofNOsynthase(NOS)particularly in bronchial epithelial cells (9). Recently,upregulationofinducibleNOS(iNOS)withintheairwayswasdemonstratedafterbronchialallergenchallenge(10),confirmingtheassociationbetweenupregulationofiNOSand increase in bronchial inflammation. The inducibleisoformofNOSisanenzymethatiscapableofproducinglargeamountsofNOandisexpressedonlyafterinductionby immunologic and inflammatory stimuli (11). Bycontrast,theconstitutiveisoformofNOS(cNOS)produ-cesonlysmallamountsofNO.ThelargequantitiesofNOthat are produced by iNOS possibly are deleterious inallergicairwaydisease.InastudyinovalbuminsensitizediNOS-knockoutmicetherewaslesseosinophilaccumu-lationinthelungs afterovalbumin challenge comparedBackground:Nitricoxideinexhaledair(eNO)iselevatedinallergicasthmacomparedwithhealthysubjectsandhasbeenproposedasamarkerofbronchialinflammation.However,eNOiselevatedtoalesserextentinallergicnon-asthmaticrhinitisaswell.Consideringthedistinctiveclinicalappearancesofbothallergicdiseases,differencesineNOareexpectedtopersistafterallergenexposure.Theaimofthestudywastocompareallergen-inducedchangesineNOinhousedustmitesensitizedpatientswithasthmaandpatientswithperennialrhinitiswithoutasthmasymptoms.Methods:Bronchialallergenchallengewasperformedin52patientssensitizedtohousedustmite(Dermatophagoidespteronyssinus),ofwhom26hadnon-asthmaticrhinitisand26hadasthma.LevelsofeNOweremeasuredbeforeand1h,1dayand1weekafterchallenge.Results:AtbaselineeNOwassignificantlylowerinnon-asthmaticrhinitiscomparedwithasthma(geometricmeaneNO(SEM):121(1.1)innon-asthmaticrhinitisvs197(1.1)nl/mininasthma,P |
| Databáze: | OpenAIRE |
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