Effects after inhalation of (1 -> 3)-beta-D-glucan in healthy humans

Citation
J. Thorn et al., Effects after inhalation of (1 -> 3)-beta-D-glucan in healthy humans, MEDIAT INFL, 10(4), 2001, pp. 173-178
Citations number
31
Categorie Soggetti
Immunology
Journal title
MEDIATORS OF INFLAMMATION
ISSN journal
09629351 → ACNP
Volume
10
Issue
4
Year of publication
2001
Pages
173 - 178
Database
ISI
SICI code
0962-9351(200108)10:4<173:EAIO(->2.0.ZU;2-B
Abstract
Background and aim: This study was performed to assess the effects of an ex posure to a pure (1 -->3)-beta -D-glucan, a cell wall component of fungi, p lants and certain bacteria. Methods: Twenty-one healthy subjects inhaled saline or (1 -->3)-beta -D-glu can suspended in saline in a random, double-blind, cross-over design. They were examined before exposure and 24 and 72 h afterwards with spirometry, b lood sampling and collection of induced sputum. Differential cell counts an d eosinophilic cationic protein (ECP) were determined in blood and sputum, and myeloperoxidase (MPO), tumour necrosis factor-alpha (TNF-alpha), and in terleukin (IL)-8 and IL-10 were determined in sputum supernatants. TNF-alph a was determined after cultivation of blood mononuclear cells. Results: In sputum, inhalation of saline caused a significant increase in E CP and TNF-alpha. (1 -->3)-beta -D-Glucan inhalation caused a further incre ase in these cytokines, although not statistically significantly different from the increase induced by inhalation of saline alone. in blood, the numb er of eosinophils was significantly decreased 72 h after the challenge with (1 -->3)-beta -D-glucan. This effect was not found after the inhalation of saline alone. TNF-alpha production from stimulated blood mononuclear cells was significantly decreased 72 h after the (1 -->3)-beta -D-glucan Inhalat ion as compared with the increase induced by saline inhalation. Conclusions: The results suggest that (1 -->3)-beta -D-glucan causes a diff erent type of response as compared with inflammatory agents such as bacteri al endotoxin that cause a neutrophil-dominated inflammatory response.