Open AccessBronchial angiogenesis in severe glucocorticoid‐dependent asthma
Author(s) -
Vrugt B.,
Wilson S,
Bron A.,
Holgate S.t,
Djukanovic R,
Aalbers R
Publication year - 2000
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.2000.01507.x
Subject(s) - asthma , cell adhesion molecule , immunohistochemistry , intercellular adhesion molecule 1 , monoclonal antibody , angiogenesis , neovascularization , intercellular adhesion molecule , glucocorticoid , medicine , vcam 1 , pathology , icam 1 , antigen , adhesion , cell adhesion , immunology , antibody , chemistry , organic chemistry
To examine the role of the bronchial microvasculature and adhesion molecule expression in severe asthma, the authors have performed an immunohistochemical study on bronchial biopsies comparing 15 glucocorticoid‐dependent asthmatics, 15 mild asthmatics and eight control subjects. Serially cut glycol methacrylate‐embedded sections were stained with monoclonal antibodies identifying the vessel marker EN‐4, intercellular adhesion molecule (ICAM)‐1, vascular cell adhesion molecule (VCAM)‐1, E‐ and P‐selectin. Sections were also stained for lymphocyte function associated antigen (LFA)‐1 and very late antigen (VLA)‐4. By comparison with mild asthma and nonasthma, severe asthma was characterized by increased numbers of submucosal vessels (p=0.009) which was associated with increased numbers of vessels expressing ICAM‐1 (p=0.005). A highly significant correlation was found between the total number of EN‐4+ vessels and the vessels expressing ICAM‐1 (r=0.85, p=0.01). In contrast, E‐selectin expression was lower in severe as compared with mild asthma (p=0.01) but not different from normal. No differences were found between the three groups in the expression of VCAM‐1 and P‐selectin nor in numbers of LFA‐1+ and VLA‐4+ cells. The results of this study support the notion that mucosal neovascularization is an important feature of airways remodelling in severe asthma. This is associated with a relatively higher density of vessels expressing intercellular adhesion molecule‐1, although the expression of this adhesion molecule per vessel was not raised.