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From the Department of Anatomy and Cardiovascular Research
Institute,*
University of California, San Francisco,
California; and the Department of Anatomy,
Kumamoto University School of Medicine, Kumamoto, Japan
We sought to determine whether the changes in microvascular endothelial cells (EC) caused by a polarized chronic inflammatory stimulus depend on proximity to the stimulus. C3H mice were infected with Mycoplasma pulmonis, which attaches to the airway epithelium and creates a polarized inflammatory stimulus across the airway wall. At 1, 2, or 4 weeks, the tracheal vasculature was stained by perfusion of silver nitrate to mark EC borders or biotinylated Lycopersicon esculentum lectin to label the EC surface and adherent leukocytes. E-selectin immunoreactivity and EC proliferation were also localized. We found that the size, shape, and immunoreactivity for adhesion molecules on EC nearest the airway lumen (subepithelial EC) were different from those on the opposite surface of the same vessels. Subepithelial EC were smaller, more irregular in shape, had greater E-selectin immunoreactivity, and had twice as many adherent leukocytes. In contrast, proliferating EC were uniformly distributed around the vessel circumference. We conclude that the polarized stimulus created by M. pulmonis infection differentially changes the size, shape, and function of EC nearest the airway epithelium. This heterogeneity may result from a gradient of inflammatory mediators that triggers the influx of leukocytes into the airway lumen.
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