Source: Annual Congress 2001 - Molecular and cellular pathology of asthma
Disease area: Airway diseases

Abstract

Introduction: In a mouse model of asthma, it has been shown that interleukin- (IL-) 18 enhanced antigen-induced airway eosinophilia. However, there is no evidence of IL-18 secretion in human airways available to date.
Methods: Segmental allergen provocation (SAP) was performed on 9 allergic asthmatics as follows: Two segments of the lung were challenged with allergen (S5 and S10 right) or saline (S5 and S6 left). A bronchoalveolar lavage (BAL) was performed at 10 min and 18 h after challenge. The concentration of IL-18 in the BAL fluid was analysed by ELISA. Cytological analysis was carried out using cyto-centrifugation and May-Gruenwald-Giemsa staining.
Results: At 10 min after segmental challenge the IL-18 concentration in BAL fluid exhibited no difference between the control and challenged segments (control: 12.46 ±] 4.03 pg/ml, challenged: 12.91 ±] 3.76 pg/ml). At 18h after allergen challenge, however, the IL-18 concentration declined in the control segment to 9.59 ±] 2.55 pg/ml and increased in the allergen challenged segment to 19.25 ±] 6.54 pg/ml. The eosinophil numbers increased from 0.39 ±] 0.11 x 10²/ml to 3.28 ±] 2.31 x10²/ml in the control segment and from 0.25 ±] 0.09 x 10²/ml to 19.20 ±] 8.60 x 10²/ml in the allergen challenged segment. There was no correlation between the concentration of IL-18 and numbers of eosinophils, neutrophils, macrophages, and lymphocytes.
Conclusion: The data show that allergen challenge causes an increase of IL-18 concentration in asthma. However, IL-18 may not play a role for infiltration and accumulation of inflammatory cells in the airways.

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Citations should be made in the following way:
M. Foerster, R. K. Braun, D. Haefner, G. Workalemahu, B. Mock, C. Kroegel (Jena, Germany). Evidence for secretion of IL-18 in asthmatic airway inflammation assessed by endobronchial allergen challenge and its relationship to accumulation of inflammatory cells. Eur Respir J 2001; 16: Suppl. 31, 3566

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