(1 →3)- β -D-Glucan and endotoxin modulate immune response to inhaled allergen. Issue 2 (1998)

• Record Type: Journal Article
• Authors: Rylander Rylander, R. R.; Holt Holt, P. G. P. G.
• Is Part Of: Mediators of inflammation. Volume 7:Issue 2(1998)
• Page Start: 105
• Page End: 110
• Publication Date: 1998
• Subjects: (1→3)-β-D-glucan -- Endotoxin -- T-cells -- Eosinophils -- Inflammation; Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1080/09629359891252
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Exposure to dust may involve co-exposure to agents which are allergens, together with those which are pro-inflamm atory. To study the effects of such a coexposure, the humoral and inflammatory responses were studied in guinea pigs inhaling the T-cell dependent antigen ovalbumin (OVA) and the inflammatory agents( 1 → 3 ) -β -D-glucan and lipopolysaccharide (LPS). The effects were evaluated as inflammatory cells in the lung and serum antibodies to OVA. LPS caused a stimulation of the OVA-induced antibody production which was abolished by simultaneous exposure to( 1 → 3 ) -β-D-glucan. An increase of eosinophils after OVA exposure was decreased by coexposure to( 1 → 3 ) -β-D-glucan. The results demonstrate a complex interaction between adaptive and innate immune mechanisms in the lung, determined by exposure to common contaminants in airborne dust.