Microvascular Remodelling In Chronic Airway Inflammation In Mice

Clinical and Experimental Pharmacology and Physiology - Tập 27 Số 10 - Trang 836-841 - 2000
Gavin Thurston1, Kevin Maas1, Allyson LaBarbara1, John W. McLean1, Donald M. McDonald1
1Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco, California, USA

Tóm tắt

SUMMARY1. 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.

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Tài liệu tham khảo

FolkmanJ&BremH.Angiogenesis and inflammation. In: Gallin JI Goldstein IM Snyderman R (eds).Inflammation: Basic Principles and Clinical Correlates 2nd edn. Raven Press New York. 1992; 821–39.

10.1096/fasebj.11.6.9194526

JacksonJR BologneseB KircherCH MarshallLA WinklerJD.Modulation of angiogenesis in a model of chronic inflammation.Inflamm. Res.1997;46(Suppl. 2): S129–30.

10.1136/jcp.13.1.27

10.1164/ajrccm.156.1.9607066

10.1111/1523-1747.ep12485169

10.1183/09031936.97.10051173

10.1016/S0002-9440(10)65654-4

10.1016/S0002-9440(10)65104-8

ThurstonG BalukP McDonaldDM.Determinants of endothelial cell phenotype in venules.Microcirculation2000;7: 67–80.

10.1164/ajrccm.150.5.7524980

10.1177/10454411950060030501

Baluk P, 1997, Upregulation of substance P receptors in angiogenesis associated with chronic airway inflammation in rats., Am. J. Physiol., 273, L565

10.1002/jcp.1041550315

10.1111/j.1476-5381.1996.tb15578.x

10.1055/s-2008-1043962

10.1016/S0022-3476(09)90024-5

10.1016/0167-4889(95)00155-7

10.1172/JCI965

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Thông tin xuất bản

Clinical and Experimental Pharmacology and Physiology

Tập 27 Số 10

836-841

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