Early decrease in nasal eosinophil proportion after nasal allergen challenge correlates with baseline bronchial reactivity to methacholine in children sensitized to house dust mites.
BACKGROUND
Allergic rhinitis is induced by an IgE mediated inflammation after allergen exposure of the membranes lining the nose which, in predisposed individuals, may constitute a risk factor for the occurrence of asthma.


OBJECTIVE
To detect early changes in nasal inflammation after allergen exposure, 11 children [9.0 (7, 11) yrs], sensitized to house dust mites (HDM), with rhinoconjunctivitis and asthma and an age- and gender-matched control group (Ctr) were studied.


METHODS
The following parameters were evaluated: i) pulmonary function; ii) bronchial reactivity to methacholine (MCh), expressed as Pd20MCh; iii) nasal brushing (NB) 'at baseline' and, on a separate day, 30 min after nasal allergen challenge (NAC). On NBs, the following markers of inflammation were evaluated: a) neutrophil and eosinophil proportion, b) 'intact to degranulated eosinophil' ratio, and c) expression of intercellular adhesion molecule (ICAM)-1 and HLA-DR by nasal epithelial cells.


RESULTS
'At baseline', allergic children showed elevated nasal eosinophilia and increased ICAM-1 and HLA-DR expression (p<0.05), as compared to Ctr. In allergic children, nasal eosinophilia correlated with Pd20MCh (p=0.002). The significant decrease in nasal eosinophilia observed after NAC (p=0.002) was associated with a significant decrease in the 'intact to degranulated eosinophil' ratio (p=0.001). Interestingly, correlations were still present between Pd20MCh and 'post NAC' eosinophilia (p=0.004) or the NAC-induced decrease in eosinophilia (p=0.010).


CONCLUSIONS
In children sensitized to HDM, experimental allergen exposure is followed by an early depletion of nasal eosinophils. The correlation between allergen-induced changes in nasal eosinophilia and bronchial reactivity to MCh further supports the concept of a tight link between upper and lower respiratory tract involvement in respiratory allergy.
Silvestri
M
M
Pulmonary Dept, G Gaslini Institute, Genoa, Italy.
Battistini
E
E
Defilippi
A C
AC
Sabatini
F
F
Sale
R
R
Pecora
S
S
Rossi
G A
GA
D000485:Allergens / Q000276:immunology; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000276:immunology; D016085:Bronchoconstrictor Agents / Q000494:pharmacology; D016022:Case-Control Studies; D002648:Child; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007958:Leukocyte Count; D008297:Male; D016210:Methacholine Chloride / Q000494:pharmacology; D009297:Nasal Mucosa / Q000276:immunology / Q000378:metabolism; D009299:Nasal Provocation Tests; D009504:Neutrophils / Q000276:immunology; D039981:Pyroglyphidae / Q000276:immunology*; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology*
D000485:Allergens; D016085:Bronchoconstrictor Agents; D006684:HLA-DR Antigens; D016210:Methacholine Chloride; D018799:Intercellular Adhesion Molecule-1; D007073:Immunoglobulin E