Expression of adhesion molecules in allergic lung diseases.
Endothelial adherence and migration of leukocytes into tissue is mediated by different sets of adhesion molecules. The expression of these sets might not only preselect the types of leukocytes that enter the inflammatory sites, but also activate these leukocytes, induce adherence to epithelial cells, and cause the release of cytokines. Atopic asthma, extrinsic allergic alveolitis, and sarcoidosis as examples of immunologic lung diseases were investigated for the expression of adhesion molecules. Bronchial biopsies in chronic obstructive lung disease (COPD) and resected lung tissue of juvenile emphysema were chosen for controls. Immunohistochemistry was done on sections from bronchial and transbronchial biopsies and on smears from bronchoalveolar lavage cells. In all three types of immune disorders, lymphocytes expressed the integrins alpha4/beta1 (VLA4) and ICAM3, whereas lymphocytes in COPD bronchitis and in emphysema controls were unreactive. Eosinophils in atopic asthma bronchitis in contrast to COPD bronchitis also expressed both VLA4 and ICAM3. The expression of VCAM1 on endothelial cells was only seen in atopic asthma and was related to disease activity. The expression of other adhesion molecules was nonspecific. Expression of VCAM1 on endothelial cells and its ligand VLA4 on lymphocytes and eosinophils seems to be a specific event in atopic asthma. Expression of VLA4 and ICAM3 on lymphocytes, however, might be a specific event in all three immune reactions.
Popper
Helmut H
HH
Institute of Pathology, Laboratory of Environmental and Respiratory Pathology, University of Graz, Auenbruggerplatz 25, 8036 Graz, Austria, Austria.
Pailer
Sabine
S
Institute of Pathology, Laboratory of Environmental and Respiratory Pathology, University of Graz, Auenbruggerplatz 25, 8036 Graz, Austria, Austria.
Wurzinger
Gerd
G
II Internal and Pulmonary Deptartments, General Hospital, Graz, Austria, Austria.
Feldner
Herwig
H
Hospital of the SVB, Gleichenberg, Austria, Austria.
Hesse
Christian
C
II Internal and Pulmonary Deptartments, General Hospital, Graz, Austria, Austria.
Eber
Eva
E
Pulmonary Hospital, Enzenbach, Austria, Austria.
D000542:Alveolitis, Extrinsic Allergic / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015703:Antigens, CD; D000943:Antigens, Differentiation; D001249:Asthma / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D001980:Bronchi / Q000378:metabolism / Q000473:pathology; D018893:Bronchoalveolar Lavage; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis*; D004727:Endothelium / Q000378:metabolism / Q000473:pathology; D004804:Eosinophils / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D039041:Integrin alpha4beta1; D016023:Integrins / Q000096:biosynthesis*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000378:metabolism; D011656:Pulmonary Emphysema / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016201:Receptors, Lymphocyte Homing / Q000096:biosynthesis*; D020545:Respiratory Mucosa / Q000378:metabolism / Q000473:pathology; D012507:Sarcoidosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
D015703:Antigens, CD; D000943:Antigens, Differentiation; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human; D039041:Integrin alpha4beta1; D016023:Integrins; D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; D016201:Receptors, Lymphocyte Homing; D018799:Intercellular Adhesion Molecule-1