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Immuno‐regulatory cytokines in asthma: IL‐15 and IL‐13 in induced sputum
Author(s) -
KomaiKoma M.,
McKay A.,
Thomson L.,
McSharry C.,
Chalmers G. W.,
Liew F. Y.,
Thomson N. C.
Publication year - 2001
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2001.01174.x
Subject(s) - sputum , immunology , cytokine , asthma , medicine , interleukin , pathology , tuberculosis
Background The importance of Th2‐type lymphocyte function in asthmatic airway inflammation is well recognized, but less is known about the factors which regulate the function of these lymphocytes in asthma. The macrophage‐derived cytokine, interleukin (IL)‐15 has a number of T cell regulatory properties which might be of relevance to asthma and its treatment. Objective The aims were to identify and quantify the T cell regulatory cytokine IL‐15 in induced sputum samples from asthmatic patients, in comparison with IL‐13, and to relate the levels of these cytokines to treatment with inhaled steroids. Methods Induced sputum was collected from 16 asthmatics (eight steroid and eight non‐steroid treated) and eight normal controls. IL‐15 and IL‐13 levels were measured by enzyme‐linked immunoassay (ELISA) in sputum. IL‐15 levels were also measured in sputum cell culture supernatants and localized to specific sputum cells by immuno‐cytochemistry. Results IL‐15 levels were increased and IL‐13 levels were decreased in sputum fluid from steroid‐treated compared with non‐steroid‐treated asthmatics. IL‐15 was localized specifically to macrophages and the proportion of these cells expressing IL‐15 correlated with sputum fluid IL‐15 and IL‐15 levels in cell culture supernatants, and all were higher in the steroid‐treated asthmatics. Conclusion IL‐15 and IL‐13 production appears to be reciprocally regulated by steroid therapy in asthma patients. The steroid‐associated increase in IL‐15 may regulate a fundamental shift away from an inflammatory Th2‐type environment in asthma and may be an essential component of the cytokine modulation underlying the therapeutic benefit of corticosteroids in this condition.