Effect and mechanism of lipopolysaccharide on allergen-induced interleukin-5 and eotaxins production by whole blood cultures of atopic asthmatics

Interleukin (IL)-5 and eotaxin families regulate the development of eosinophilic inflammation of asthma in a co-operative manner. The exposure to airborne lipopolysaccharide (LPS) induces varying degrees of airflow obstruction and neutrophilic airway inflammation. Production of IL-5 and eotaxin subf...

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Bibliographic Details
Published in:Clinical and Experimental Immunology 2007-03, Vol.147 (3), p.440-448
Main Authors: Min, J.-W, Park, S.-M, Rhim, T.Y, Park, S.-W, Jang, A.-S, Uh, S.-T, Park, C.-S, Chung, I.Y
Format: Article
Language:English
Subjects:
Adult
Allergens - immunology
Antigens, Dermatophagoides - immunology
asthma
Asthma - immunology
Asthma - physiopathology
Biological and medical sciences
Cells, Cultured
Chemokine CCL11
Chemokine CCL24
Chemokines, CC - biosynthesis
Chemokines, CC - blood
Clinical Studies
D.p. antigen
Dermatophagoides pteronyssinus
Dose-Response Relationship, Immunologic
eotaxin-2
Female
Forced Expiratory Volume
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Humans
Immunoglobulin E - blood
Immunopathology
interleukin-10
Interleukin-10 - immunology
interleukin-5
Interleukin-5 - biosynthesis
Interleukin-5 - blood
Lipopolysaccharides - immunology
LPS
Male
Medical sciences
Reverse Transcriptase Polymerase Chain Reaction - methods
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Summary:Interleukin (IL)-5 and eotaxin families regulate the development of eosinophilic inflammation of asthma in a co-operative manner. The exposure to airborne lipopolysaccharide (LPS) induces varying degrees of airflow obstruction and neutrophilic airway inflammation. Production of IL-5 and eotaxin subfamily chemokines was analysed in response to Dermatophagoides pteronyssinus allergen (D.p.) according to the presence of specific IgE to D.p., and investigated the mechanism underlying their LPS-mediated regulation of these cytokines in response to the specific allergen. Peripheral blood cells (PBCs) from asthmatics with (group 1) or without (group 2) specific IgE to D.p. and from non-asthmatics with (group 3) or without (group 4) were stimulated with D.p. or LPS. For LPS-mediated inhibition of IL-5 and eotaxin-2 production, LPS-induced cytokines were added to the D.p.-stimulated PBCs. IL-5 and eotaxin-2, but not eotaxin-1 and 3, were significantly increased by D.p.-stimulated-PBCs from group 1, while only eotaxin-2 was elevated in group 3. Eotaxin-2 production was found in monocytes and correlated with the level of specific IgE to D.p. LPS treatment resulted in the decrease in eotaxin-2 and IL-5 production by the D.p.-stimulated PBCs. LPS-induced IL-10 completely inhibited D.p.-stimulated production of eotaxin-2 and IL-5. The differential responses of the eotaxin family to specific antigens suggest that the predominant role of eotaxin-2 and LPS may attenuate eosinophilic inflammation by inhibiting IL-5 and eotaxin-2 synthesis through IL-10 production.
ISSN:0009-9104
1365-2249
1365-2567
DOI:10.1111/j.1365-2249.2006.03294.x