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Cytokine profiles in asthma families depend on age and phenotype.

PLoS ONE 5:e14299 (2010)
Verlagsversion Volltext DOI
Open Access Gold
Creative Commons Lizenzvertrag
Circulating cytokine patterns may be relevant for the diagnosis of asthma, for the discrimination of certain phenotypes, and prognostic factors for exacerbation of disease. METHODOLOGY/PRINCIPAL FINDINGS: In this study we investigated serum samples from 944 individuals of 218 asthma-affected families by a multiplex, microsphere based system detecting at high sensitivity eleven asthma associated mediators: eotaxin (CCL11), granulocyte macrophage stimulating factor (GM-CSF), interferon gamma (IFNγ), interleukin-4 (IL-4), IL-5, IL-8, IL-10, IL-12 (p40), IL-13, IL-17 and tumor necrosis factor alpha (TNFα). Single cytokine levels were largely similar between asthmatic and healthy individuals when analysing asthma as single disease entity. Regulatory differences between parental and pediatric asthma were reflected by six of the eleven mediators analyzed (eotaxin, IL-4, IL-5, IL-10, IL-12, TNFα). IL-12 (p40) and IL-5 were the best predictor for extrinsic asthma in children with an increased odds ratio of 2.85 and 1.96 per log pg/ml increase (IL-12 (p40): 1.2-6.8, p=0.019, and IL-5: 1.2-2.5, p=0.025). Frequent asthma attacks in children are associated with elevated IL-5 serum levels (p=0.013). Cytokine patterns seem to be individually balanced in both, healthy and diseased adults and children, with various cytokines correlating among each other (IL-17 and IFNγ (rs=0.67), IL-4 and IL-5 (rs=0.55), IFNγ and GM-CSF (rs=0.54)). CONCLUSION/SIGNIFICANCE: Our data support mainly an age- but also an asthma phenotype-dependent systemic immune regulation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter NECROSIS-FACTOR-ALPHA; COLONY-STIMULATING FACTOR; SERUM INTERFERON-GAMMA; ATOPIC ASTHMA; T-CELLS; PROINFLAMMATORY CYTOKINES; AIRWAY INFLAMMATION; LUNG-FUNCTION; INTERLEUKIN-8; LYMPHOCYTES
ISSN (print) / ISBN 1932-6203
Zeitschrift PLoS ONE
Quellenangaben Band: 5, Heft: 12, Seiten: , Artikelnummer: e14299 Supplement: ,
Verlag Public Library of Science (PLoS)
Verlagsort Lawrence, Kan.
Begutachtungsstatus Peer reviewed