Original article Nasal inflammation and bronchial reactivity to methacholine in atopic children with respiratory symptoms Inpredisposedindividuals,allergicrhinitismayconstitute a risk factor for the occurrence of asthma (1, 2) being stronger for patients sensitized to house dust mites (HDM) than for those sensitized to pollens (3, 4). The concept that, at least in atopy, upper and lower airways should be considered a unique entity influenced by common physiologic processes (1, 4) is supported by recent studies showing tight similarities in tissue inflam- matory changes in asthma and rhinitis (4, 5). However, differences may exist at these two levels (i.e. bronchi and nose) in the extent of the inflammatory changes and in the involvement of the inflammatory cell productsinproducingreversibleandirreversibledamages to the parenchymal structures (5). In asthma, eosinophilic bronchial inflammation, which may be present also in asymptomatic asthmatic individ- uals, correlates with baseline lung function and with the increaseinairwayhyperresponsivenessfollowingallergen challenge (6, 7). Although it is not known whether this ‘subclinical’recruitmentandactivationofleukocytesmay lead to irreversible airway remodelling, it has been suggested that evaluation of airway inflammation, together with measurement of pulmonary function, may be useful to identify individuals who may need a closer follow-up and/or a more aggressive treatment (7). Inthiscontext,itcouldbeinterestingtoknowwhether thenosecouldbeusedasawindowonthelowerairways, i.e.whetherinchildrenwithallergicrespiratorysymptoms, inflammatorychangesdetectedinthenasalmucosacould reflectthedegreeofasthmaticinvolvement,i.e.abnormal- ities in respiratory functions. Nasal brushing was per- formed in atopic children with rhinoconjunctivitis and intermittentasthmaticsymptomsandincontrol(Ctr)sub- jects:thepercentagesofeosinophils(Eos)andintercellular adhesion molecule-1 (ICAM-1) expression by epithelial Background: In atopic subjects, dysfunctions of the upper and lower airways frequently coexist and allergic rhinitis seems to constitute a risk factor for the occurrence of asthma in predisposed individuals. Aim of the study: To evaluate whether in atopic subjects nasal inflammation could reflect changes in respiratory functions, 11 allergic children, sensitized to housedustmites(HDM),withrhinoconjunctivitisandasthmaand10nonatopic controls (ctrs) were studied. Methods: All subjects underwent nasal brushing to detect percentages of nasal eosinophils(Eos%)andintercellularadhesionmolecule-1(ICAM-1)expression by nasal epithelial cells. In the same day pulmonary function tests, i.e. forced vitalcapacity(FVC),forcedexpiratoryvolumein1s(FEV 1 ), forced expiratory flows at 25–75% of the vital capacity (FEF 25)75% ) and methacholine (MCh) bronchial inhalation challenge were also evaluated. Results: Pulmonary function parameters were not significantly different in allergicchildrenandinctrs(P >0.05),whileasignificantincreaseinbronchial reactivity to MCh, expressed as Pd 20 MCh, was detected in the former popu- lation(P <0.05).Ascomparedwithctrs,allergicchildrenshowedelevatedEos % and ICAM-1 expression (P < 0.05). When nasal inflammation and pul- monaryfunctionparameterswerecompared,asignificantcorrelationwasfound between nasal Eos % and bronchial reactivity to MCh (P ¼ 0.002). Conclusions: These data support the concept of significant links between upper and lower respiratory tract involvement in atopic children sensitized to HDM. R. Sale 1 , M. Silvestri 1 , E. Battistini 1 , A.-C. Defilippi 1 , F. Sabatini 1 , S. Pecora 2 , G. A. Rossi 1 1 Pulmonary Division, G. Gaslini Institute, Genoa; 2 Alk-Abellò S.p.A., Milan, Italy Key words: adhesion molecules; atopy; bronchial hyperreactivity; eosinophils; nasal brushing. Giovanni A. Rossi, MD Pulmonary Division G. Gaslini Institute Largo G. Gaslini 5 16147 Genoa, Italy Accepted for publication 30 April 2003 Abbreviations: Ctrs, controls; Eos, eosinophils; FEF 25)75% , forced expiratory flows at 25–75% of the vital capacity; FEV 1 , forced expiratory volume in 1 s; FVC, forced vital capacity; HDM, house dust mites; ICAM-1, intercellular adhesion molecule-1; IgE, immunoglobulin E; LFA-1, lymphocyte function-associated anti- gen-1; Mac-1, macrophage antigen-1; MCh, methacholine; mfc, meanfluorescencechannel;PD20methacholine,MChdosecausing a20%decreaseinFEV 1 ;RAST,radioallergosorbenttest;SPT,skin pricktest;VCAM-1,vascularcelladhesionmolecule-1;VLA-4,very late antigen-4. Allergy 2003: 58: 1171–1175 Printed in UK. All rights reserved Copyright Ó Blackwell Munksgaard 2003 ALLERGY 1171