1. Chronic inflammation is associated with blood vessel remodelling, includ
ing vessel proliferation and enlargement, and changes in vessel phenotype.
We sought to characterize these changes in chronic airway inflammation and
to determine whether corticosteroids that inhibit inflammation, such as dex
amethasone, can also reduce microvascular remodelling.
2. Chronic airway inflammation was induced in C3H mice by infection with My
coplasma pulmonis and the tracheal vessels were examined in whole mounts af
ter Lycopersicon esculentum lectin staining.
3. Neither the number nor the length of vessels changed in C3H mice after i
nfection with M. pulmonis. Instead, vessel diameter and endothelial cell nu
mber doubled.
4. Immunoreactivity for P-selectin, a marker of venular endothelial cells,
also increased after infection, indicating that the proportion of venules d
oubled with a corresponding decrease in capillaries.
5. Whereas the average diameter of tracheal capillaries doubled in mice ino
culated 10 days earlier (mean (+/- SEM) diameter in infected and pathogen-f
ree mice of 20.8 +/- 1.6 and 9.0 +/- 0.7 mu m, respectively), dexamethasone
treatment (0.2 mg/day, i.p.) for 7 days beginning 4 days after infection s
ignificantly decreased capillary diameter (13.0 +/- 0.7 mu m). The treatmen
t also decreased the immunoreactivity for P-selectin and the number of adhe
rent leucocytes (595 +/- 203 vs 2024 +/- 393 cells/mm(2) in treated and non
-treated infected mice, respectively).
6. We conclude that microvascular enlargement and changes in vessel phenoty
pe are features of some types of chronic inflammation and, furthermore, tha
t dexamethasone reverses the microvascular enlargement, changes in vessel p
henotype and leucocyte influx associated with chronic inflammatory airway d
isease.