Increased expression of IL-16 immunoreactivity in bronchial mucosa after segmental allergen challenge in patients with asthma.
BACKGROUND
We have previously shown increased expression of the CD4(+) cell chemoattractant IL-16 in bronchial mucosa of patients with asthma. We investigated the effects of allergen challenge on airway IL-16 expression.


METHODS
We investigated the expression of IL-16 immunoreactivity in bronchial biopsy samples obtained from atopic asthmatic subjects (n = 19) and normal subjects (n = 6) 24 hours after segmental allergen challenge. Control biopsy samples were obtained either at baseline or after diluent challenge. IL-16 expression was correlated to numbers of CD4(+) cells, CD25(+) cells, and activated eosinophils. IL-16 bioactivity was assessed in bronchoalveolar fluid obtained from patients with asthma.


RESULTS
IL-16 expression was higher in control biopsy specimens obtained from subjects with asthma compared with normal subjects (P<.05). In patients with asthma, numbers of IL-16 immunoreactive cells were significantly higher in biopsy specimens obtained after allergen challenge compared with control biopsy specimens (P<.001). Allergen provocation was associated with release of IL-16 in bronchoalveolar fluid in patients with asthma. In normal subjects, there was no difference in the number of IL-16-immunoreactive cells in biopsy specimens obtained after allergen challenge compared with biopsy specimens obtained after diluent challenge. Allergen challenge was associated with an increase in the numbers of EG2(+) eosinophils in patients with asthma but not in normal subjects. IL-16 expression correlated with the numbers of CD4(+) cells and CD25(+) cells after allergen challenge in asthmatic subjects with a provocative concentration required to decrease the FEV(1) by 20% of its baseline value (PC(20)FEV(1)) < 4 mg/mL. IL-16-immunoreactive cells were identified mainly as T cells and eosinophils in asthmatic subjects after allergen challenge.


CONCLUSIONS
Endobronchial allergen provocation in atopic asthmatic patients resulted in increased airway expression of IL-16 and release of bioactive IL-16 in airways. IL-16 may contribute to the immunoregulation of the inflammatory infiltrate in the airways in response to antigen.
Laberge
S
S
Department of Pediatrics, Ste-Justine Hospital, University of Montreal, Montreal, Quebec, Canada.
Pinsonneault
S
S
Varga
E M
EM
Till
S J
SJ
Nouri-Aria
K
K
Jacobson
M
M
Cruikshank
W W
WW
Center
D M
DM
Hamid
Q
Q
Durham
S R
SR
D000328:Adult; D000485:Allergens / Q000494:pharmacology*; D001249:Asthma / Q000276:immunology*; D001980:Bronchi; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology; D002630:Chemotactic Factors / Q000378:metabolism; D004804:Eosinophils / Q000737:chemistry; D005260:Female; D006801:Humans; D019410:Interleukin-16 / Q000235:genetics / Q000276:immunology*; D018655:Lymphocyte Count; D008297:Male; D010641:Phenotype; D015375:Receptors, Interleukin-2 / Q000032:analysis; D020545:Respiratory Mucosa / Q000737:chemistry / Q000166:cytology / Q000276:immunology
D000485:Allergens; D002630:Chemotactic Factors; D019410:Interleukin-16; D015375:Receptors, Interleukin-2