Inhalation of (1 -> 3)-beta-D-glucan causes airway eosinophilia

Citation
B. Fogelmark et al., Inhalation of (1 -> 3)-beta-D-glucan causes airway eosinophilia, MEDIAT INFL, 10(1), 2001, pp. 13-19
Citations number
22
Categorie Soggetti
Immunology
Journal title
MEDIATORS OF INFLAMMATION
ISSN journal
09629351 → ACNP
Volume
10
Issue
1
Year of publication
2001
Pages
13 - 19
Database
ISI
SICI code
0962-9351(200102)10:1<13:IO(-3C>2.0.ZU;2-C
Abstract
BACKGROUND: Moulds are present in a variety of environments and aerosols of fungal spores are generated when mouldy materials are handled. Molds conta in (1-->3)-beta -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 res ponse in the lung after inhalation of (1-->3)-beta -D-glucan and bacterial endotoxin. Methods: Guinea pigs were exposed daily to an aerosol of pure (1-->3)-beta -D-glucan and pure endotoxin for five weeks. Lung lavage and lung interstit ial cell preparations were done and the inflammatory cells counted. Histolo gical sections were prepared from the trachea. Results: There was an increase in eosinophil numbers in lung lavage, lung i nterstitium, and the airway epithelium of animals exposed to (1-->3)-beta - D-glucan. In animals simultaneously exposed to endotoxin, there was no incr ease in eosinophils. In the lung interstitium, (1-->3)-beta -D-glucan expos ure caused an increase in lymphocytes, which was not found after endotoxin exposure. Endotoxin exposure caused an increase in neutrophils and macropha ges in lung lavage, which was not found after (1-->3)-beta -D-glucan exposu re. Conclusions: The results support previous findings that (1-3)-beta -D-gluca n causes a different response in the airways as compared to endotoxin. Endo toxin modulated the increase in eosinophils caused by (1-->3)-beta -D-gluca n exposure, suggesting a complex interaction between the microbial cell wal l components.