PMID- 1682272
OWN - NLM
STAT- MEDLINE
DCOM- 19911223
LR  - 20190816
IS  - 0020-5915 (Print)
IS  - 0020-5915 (Linking)
VI  - 94
IP  - 1-4
DP  - 1991
TI  - Potential implication of endothelial cells in bronchial asthma.
PG  - 233-8
AB  - Inflammatory cells like eosinophils, neutrophils or mononuclear phagocytes have 
      long been recognized as essential components in the pathophysiology of asthma. 
      After recruitment in situ and subsequent activation, they are considered as 
      responsible for epithelial and submucosal bronchial alterations. However, to 
      access to the inflammatory site, these cells have to cross the endothelial wall, 
      suggesting so a potential implication of endothelial cells (EC) in bronchial 
      asthma. To test this hypothesis, we studied in a first step the modulation of 
      vascular adhesions like intercellular adhesion molecule-1 (ICAM-1) on EC: 
      supernatants of alveolar macrophages (AM) recovered by bronchoalveolar lavage in 
      patients exhibiting a late asthmatic reaction, induced an enhanced expression of 
      ICAM-1 on EC preparations; increase of ICAM-1 was clearly correlated to amounts 
      of tumor necrosis factor-alpha (TNF alpha) present in AM supernatants, as shown 
      by inhibition experiments with anti-TNF alpha antiserum. The second way to 
      explore the possible role of EC in asthma was the detection of autoantibodies to 
      EC in various allergic disorders: antibodies against a 120-kD EC antigen in 
      patients with allergic granulomatosis and angiitis, antibodies towards a 55-kD 
      component, common to human EC and platelets in patients with severe asthma, 
      namely characterized by their corticosteroid dependence or by aspirin-induced 
      intolerance. So our data suggest that bronchial asthma might result from either 
      EC activation, through the induction of surface adhesion molecules or from an 
      autoimmune process involving EC antigens.
FAU - Lassalle, P
AU  - Lassalle P
AD  - Centre d'Immunologie et Biologie Parasitaire Institut Pasteur, Lille, France.
FAU - Delneste, Y
AU  - Delneste Y
FAU - Gosset, P
AU  - Gosset P
FAU - Tonnel, A B
AU  - Tonnel AB
FAU - Capron, A
AU  - Capron A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Int Arch Allergy Appl Immunol
JT  - International archives of allergy and applied immunology
JID - 0404561
RN  - 0 (Autoantibodies)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Angioedema/immunology
MH  - Asthma/*etiology/immunology
MH  - Autoantibodies/analysis
MH  - Cell Adhesion Molecules/analysis
MH  - Endothelium/immunology/*physiology
MH  - Eosinophilia/immunology
MH  - Female
MH  - Humans
MH  - Intercellular Adhesion Molecule-1
MH  - Lymphocyte Activation
MH  - Male
MH  - Middle Aged
MH  - Tumor Necrosis Factor-alpha/physiology
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
AID - 10.1159/000235368 [doi]
PST - ppublish
SO  - Int Arch Allergy Appl Immunol. 1991;94(1-4):233-8. doi: 10.1159/000235368.