M. Sjostrand et R. Rylander, PULMONARY CELL INFILTRATION AFTER CHRONIC EXPOSURE TO (1-]3)-BETA-D-GLUCAN AND CIGARETTE-SMOKE, Inflammation research, 46(3), 1997, pp. 93-97
Objective and Design: To evaluate the effect of a microbial cell wall
component-(1-->3)-beta-D-glucan-on the inflammatory effect induced by
cigarette smoke in a subchronic exposure situation. Material: Groups o
f guinea-pigs were exposed 5 days/week to cigarette smoke, an aerosol
of (1-->3)-beta-D-glucan, or to both. Methods: The numbers of differen
t inflammatory cells were studied in histological sections, enzyme dig
ested lung tissue and in lung lavage. Cell enzyme production was measu
red. Results: Exposure to (1-->3)-beta-D-glucan or cigarette smoke cau
sed only minor alterations in inflammatory cells. Given together they
caused an increase in cellularity in the tissue with significantly inc
reased numbers of macrophages, lymphocytes, neutrophils and eosinophil
s. There was also an increase in subepithelial eosinophils. Lung lavag
e cell enzyme production was slightly lower in the combined exposure g
roup. Conclusion: The results demonstrate that (1-->3)-beta-D-glucan s
ynergistically increases the inflammation induced by cigarette smoke.
The mechanism may be a downregulation of the macrophage control of inf
lammatory cell migration into the lung tissue.