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Effects after inhalation of (1→3)-β -D-glucan in healthy humans

Background and aim: This study was performed to assess the effects of an exposure to a pure (1→ 3)-β -D-glucan, a cell wall component of fungi, plants and certain bacteria. Methods: Twenty-one healthy subjects inhaled saline or (1→ 3)- β-D-glucan suspended in saline in a random, double-blind, cross-...

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Bibliographic Details
Published in:Mediators of Inflammation 2001-08, Vol.2001 (4), p.173-178
Main Authors: Thorn, J, Beijer, L, Rylander, R
Format: Article
Language:English
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Summary:Background and aim: This study was performed to assess the effects of an exposure to a pure (1→ 3)-β -D-glucan, a cell wall component of fungi, plants and certain bacteria. Methods: Twenty-one healthy subjects inhaled saline or (1→ 3)- β-D-glucan suspended in saline in a random, double-blind, cross-over design. They were examined before exposure and 24 and 72 h afterwards with spirometry, blood sampling and collection of induced sputum. Differential cell counts and eosinophilic cationic protein (ECP) were determined in blood and sputum, and myeloperoxidase (MPO), tumour necrosis factor-a (TNF-α ), and interleukin (IL)-8 and IL-10 were determined in sputum supernatants. TNF-α was determined after cultivation of blood mononuclear cells. Results: In sputum, inhalation of saline caused a significant increase in ECP and TNF-α . (1→ 3)- β-D-Glucan inhalation caused a further increase in these cytokines, although not statistically significantly different from the increase induced by inhalation of saline alone. In blood, the number of eosinophils was significantly decreased 72 h after the challenge with (1→ 3)- β-D-glucan. This effect was not found after the inhalation of saline alone. TNF-α production from stimulated blood mononuclear cells was significantly decreased 72 h after the (1→ 3)- β-D-glucan inhalation as compared with the increase induced by saline inhalation. Conclusions: The results suggest that (1→ 3)- β-D-glucan causes a different type of response as compared with inflammatory agents such as bacterial endotoxin that cause a neutrophil-dominated inflammatory response.
ISSN:0962-9351
1466-1861
DOI:10.1080/09629350120080366