Microvascular Remodelling In Chronic Airway Inflammation In Mice

• Published in: Clinical and Experimental Pharmacology and Physiology Vol. 27; no. 10; pp. 836 - 841
• Main Authors: Thurston, Gavin, Maas, Kevin, LaBarbara, Allyson, McLean, John W, McDonald, Donald M
• Format: Conference Proceeding Journal Article
• Language: English
• Published: Melbourne, Australia Blackwell Science Pty 01.10.2000
• Subjects: angiogenesis; Animals; Capillary Permeability; Chronic Disease; chronic inflammation; Dexamethasone - therapeutic use; endothelial cell phenotype; Endothelium, Vascular - metabolism; Endothelium, Vascular - pathology; Glucocorticoids - therapeutic use; Leukocytes - drug effects; Leukocytes - metabolism; Male; Mice; Mice, Inbred C3H; microvessel enlargement; Mycoplasma - growth & development; Mycoplasma pulmonis; Neovascularization, Pathologic - drug therapy; Neovascularization, Pathologic - metabolism; Neovascularization, Pathologic - physiopathology; P-Selectin - metabolism; Pneumonia, Bacterial - drug therapy; Pneumonia, Bacterial - metabolism; Pneumonia, Bacterial - physiopathology; trachea; Trachea - blood supply; Trachea - metabolism; Trachea - pathology; venule
• ISSN: 0305-1870; 1440-1681
• DOI: 10.1046/j.1440-1681.2000.03342.x

SUMMARY 1. Chronic inflammation is associated with blood vessel remodelling, including 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 dexamethasone, can also reduce microvascular remodelling. 2. Chronic airway inflammation was induced in C3H mice by infection with Mycoplasma pulmonis and the tracheal vessels were examined in whole mounts after Lycopersicon esculentum lectin staining. 3. Neither the number nor the length of vessels changed in C3H mice after infection with M. pulmonis. Instead, vessel diameter and endothelial cell number doubled. 4. Immunoreactivity for P‐selectin, a marker of venular endothelial cells, also increased after infection, indicating that the proportion of venules doubled with a corresponding decrease in capillaries. 5. Whereas the average diameter of tracheal capillaries doubled in mice inoculated 10 days earlier (mean (±SEM) diameter in infected and pathogen‐free mice of 20.8±1.6 and 9.0±0.7 μm, respectively), dexamethasone treatment (0.2 mg/day, i.p.) for 7 days beginning 4 days after infection significantly decreased capillary diameter (13.0±0.7 μm). The treatment also decreased the immunoreactivity for P‐selectin and the number of adherent 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 phenotype are features of some types of chronic inflammation and, furthermore, that dexamethasone reverses the microvascular enlargement, changes in vessel phenotype and leucocyte influx associated with chronic inflammatory airway disease.