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)-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 response 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 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)-beta-D-glucan. In animals simultaneously exposed to endotoxin, there was no increase in eosinophils. In the lung interstitium, (1-->3)-beta-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)-beta-D-glucan exposure. CONCLUSIONS: The results support previous findings that (1-->3)-beta-D-glucan causes a different response in the airways as compared to endotoxin. Endotoxin modulated the increase in eosinophils caused by (1-->3)-beta-D-glucan exposure, suggesting a complex interaction between the microbial cell wall components.
The number of inflammatory cells was studied in lung walls and airways after inhalation of endotoxin or beta-1,3-glucan. In the water unsoluble form, beta-1,3-glucan caused a delayed response in terms of a decrease in macrophages and lymphocytes in the lung wall, 1 to 7 days after exposure but no invasion of neutrophils into the airways. When solubilized in 0.02 N NaOH, the cell response was the same as that observed after exposure to endotoxin.
The amount of (1-->3)-beta-D-glucan in pollen from different plants was evaluated using the Limulus assay with a specific lysate. The amount ranged from 79 to 1800 ng/10(6) pollen. A calculation of the inhaled dose suggests that the amount of (1-->3)-beta-D-glucan present during periods with a high pollen content in the air exceeds levels that cause airways inflammation.
SummaryTo test the hypothesis that airborne microbial cell wall components could induce an in¯ammatory response in the lungs, measurements were made of the am ounts of bac terial endotoxin and (1! 3)-b-D-glucan in laborat ory animal bedding materials. Groups of rat s were exposed by inhalati on to airborne endotoxin, (1! 3)-b-D-glucan or a combination of the two for 5 weeks. T he results demonstrated that measurable amounts of endotoxin and (1! 3)-b-Dglucan could be detected in the different bedding materials. In contrast to animals at delivery, those kept on bedding for 5 weeks showed moderat e in¯ammatory reactions in the lung. T hese were most pronounced among animals exposed to endotoxin and (1! 3)-b-D-glucan. T he results suggest that further studies need to be undertaken to elucidat e the role of microbial cell wall products in the development of in¯ammatory lung responses am ong research animals. Keywords Lung; in¯am mation; endotoxin; (1! 3)-b-D-glucan; bedding T he need for high-quality laboratory research anim als was realized during the 1960s and 1970s, leading to the development of control of infectious agents and to animals of de®ned microbiological qualit y. In spite of always working with high-qualit y animals, we (BE and LE) have noticed over a number of years hyperreactivity in the airways among the rats in our experimental laboratory, expressed in an increased mortality in anaesthetized animals and unusual reactions in normally well-running animal models. T hese phenomena occurred particularly during autumn. Mac roscopically, the lungs showed multiple small grey nodules. Histological sections revealed mild to moderate multifocal interstitial pneumonia, alveolar histocytosis, lymphoid cuf®ng and perivascular eosinophilia. In spite of this, the animals were free from known respiratory and general infections. Similar observations have previously been reported by Elwell e t a l. (1997).During recent years, it has become evident that an in¯ammat ory response in the lungs may, apart from infections, be caused by microbial cell wall components, particularly endotoxin from Gram-negative bac teria and (1! 3)-b-D-glucan, a cell wall component of moulds, certain bac teria and plants (Fogelmark e t a l. 1994, Fogelmark & Rylander 1997
The amount of (1→3)-β- D-glucan in three species of fungi was measured dur ing different phases of growth and after death. The amounts were the same in living and dead spores, but not related to growing time or medium. The amount of (1→3)-β- D-glucan was significantly higher in Stachybotrus than in Penicillium and Aspergillus. In view of the well known effects of (1→3)-β- D- glucan on the immune system, the results suggest that this agent may be a better indicator of risk in indoor environments than airborne viable or dead spores.
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