Mediators of Inflammation

Mediators of Inflammation / 2001 / Article

Open Access

Volume 10 |Article ID 848367 | https://doi.org/10.1080/09629350123707

Birgitta Fogelmark, Jörgen Thorn, Ragnar Rylander, "Inhalation of (1→3)-β-D-glucan causes airway eosinophilia", Mediators of Inflammation, vol. 10, Article ID 848367, 7 pages, 2001. https://doi.org/10.1080/09629350123707

Inhalation of (1→3)-β-D-glucan causes airway eosinophilia

Abstract

Background: Moulds are present in a variety of environments and aerosols of fungal spores are generated when mouldy materials are handled. Molds contain (1→3)-β-D-glucan, a polyglucose which is present in the cell wall of fungi, certain bacteria and plants.Aim: This study was undertaken to investigate the cellular inflammatory response in the lung after inhalation of (1→3)-β-D-glucan and bacterial endotoxin.Methods: Guinea pigs were exposed daily to an aerosol of pure (1→3)-β-D-glucan and pure endotoxin for five weeks. Lung lavage and lung interstitial cell preparations were done and the inflammatory cells counted. Histological sections were prepared from the trachea.Results: There was an increase in eosinophil numbers in lung lavage, lung interstitium, and the airway epithelium of animals exposed to (1→3)-β-D-glucan. In animals simultaneously exposed to endotoxin, there was no increase in eosinophils. In the lung interstitium, (1→3)-β-D-glucan exposure caused an increase in lymphocytes, which was not found after endotoxin exposure. Endotoxin exposure caused an increase in neutrophils and macrophages in lung lavage, which was not found after (1→3)-β-D-glucan exposure.Conclusions: The results support previous findings that (1→3)-β-D-glucan causes a different response in the airways as compared to endotoxin. Endotoxin modulated the increase in eosinophils caused by (1→3)-β-D-glucan exposure, suggesting a complex interaction between the microbial cell wall components.

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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