title: Effect and mechanism of lipopolysaccharide on allergen-induced interleukin-5 and eotaxins production by whole blood cultures of atopic asthmatics.
abstract: 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.
authors.affiliation: Genome Research Center for Allergy and Respiratory Diseases, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Korea.
authors.forename: J-W
authors.initials: JW
authors.lastname: Min
authors.forename: S-M
authors.initials: SM
authors.lastname: Park
authors.forename: T Y
authors.initials: TY
authors.lastname: Rhim
authors.forename: S-W
authors.initials: SW
authors.lastname: Park
authors.forename: A-S
authors.initials: AS
authors.lastname: Jang
authors.forename: S-T
authors.initials: ST
authors.lastname: Uh
authors.forename: C-S
authors.initials: CS
authors.lastname: Park
authors.forename: I Y
authors.initials: IY
authors.lastname: Chung
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology; D039741:Antigens, Dermatophagoides / Q000276:immunology; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology; D002478:Cells, Cultured; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D019742:Chemokines, CC / Q000096:biosynthesis* / Q000097:blood; D004306:Dose-Response Relationship, Immunologic; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D016753:Interleukin-10 / Q000276:immunology; D015848:Interleukin-5 / Q000096:biosynthesis* / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods
chemical_list: D000485:Allergens; D039741:Antigens, Dermatophagoides; C515456:CCL11 protein, human; C515484:CCL24 protein, human; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D019742:Chemokines, CC; D015848:Interleukin-5; D008070:Lipopolysaccharides; D016753:Interleukin-10; D007073:Immunoglobulin E