Background and Objectives: Sulfur dioxide gas is one of the major airborne pollutants noxious to human in industrialized countries. The most vulnerable areas in the human respiratory system were the trachea and main bronchi and a gradient
of
decreasing damage was observed in the peripheral tracheobronchial tree. Induced functional alteration was increased mucosal permeability, and morphological changes were epithelial sloughing, intracellular edema, mitochondrial swelling, widened
intercellular spaces, and ciliary cytoplamic extrusions.
The laminins are a family of extracellular matrix glycoproteins localized in the basement membrane. Their primary role is cell-matrix attachment, but many additional biologic activities, including promoting cell growth and migration, tumor growth
and
metastasis, wound repair, and graft survival, have been demonstrated.
Materials and Methods: Histologic changes and expression of laminin in tracheal mucosa sacrificed at 1 day, 2 day, 3 day, 1 week, 2 weeks, and 3 weeks after continued SO2 exposure of 250 ppm for 30 minutes a day (to 7 week) were
studied in rats.
In this study, mild immune reaction for laminin was noted at the apical cytoplasm of epithelial cells and basement membrane one day after a 7 week SO2 exposure. The cilia and nucleoi of epithelial cells were normal and no immune
reaction
was
noted in Goblet cells. The laminia propria of the tracheal tissue was infiltrated by monocytes and lymphocytes.
Results: At 24 hours after exposure, all tracheal cells except Goblet cells revealed a mild immune reaction for laminin. No immune reactions were noted in the basement membrane. At 72 hours after exposure, mild or moderate immune reactions
for
laminin was seen in the tracheal cell cytoplasm. Irregular faint immune reaction for laminin was noted in the basement membrane. At 1 week after exposure, strong immune reaction for laminin was detected over all tracheal cells, and the basement
membrane
was seen clearly. At 2~3 weeks after exposure, strong immune reaction for laminin was ween in all tracheal epithelial cells except Goblet cells and a mild immune reaction was partly revealed in the basement membrane.
Conclusion: Our study suggests that SO2 produces histologic damage on the tracheal mucosa. Longer duration after exposure of SO2 makes more progressive healing on the tracheal mucosa and increased immunoreactivity for
laminin.
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