title: Vascular endothelial cadherin expression in lung specimens of patients with sepsis-induced acute respiratory distress syndrome and endothelial cell cultures.
abstract: OBJECTIVE
  Vascular endothelial (VE) cadherin is a cell adhesion molecule localized at endothelial cell (EC) junctions. As a major component of endothelial adherens junctions, its main function is the maintenance and regulation of EC integrity. In the acute respiratory distress syndrome (ARDS), increased vascular permeability is a major mechanism in pulmonary edema and lung dysfunction. In this study, VE-cadherin expression was investigated in ARDS lungs and control tissue as well as in an ARDS cell culture model.
  
  
  METHODS
  Lung specimens of patients with ARDS due to Gram-negative sepsis (n = 20; control lung tissue: n = 41) and cell cultures of human pulmonary microvascular ECs and human umbilical vein ECs stimulated with LPS, TNF-α and IFN-γ were stained with a VE-cadherin antibody. Staining intensity was semiquantitatively evaluated by conventional light and immunofluorescence microscopy.
  
  
  RESULTS
  VE-cadherin expression was statistically significantly reduced in the endothelium of all vessel types in ARDS lungs compared to control tissue. Cell cultures showing disrupted cellular borders confirmed these results.
  
  
  CONCLUSIONS
  Reduced expression of VE-cadherin has to be considered as a major mechanism of increased vessel permeability in ARDS. The previously described vessel-type-specific expression pattern of VE-cadherin in the human lung is not influenced by ARDS.
authors: Division of Ophthalmic Pathology, Department of Ophthalmology, University of Bonn, DE-53127 Bonn, Germany.
authors: Martina C
authors: MC
authors: Herwig
authors: Michael
authors: M
authors: Tsokos
authors: M Iris
authors: MI
authors: Hermanns
authors: C James
authors: CJ
authors: Kirkpatrick
authors: Annette M
authors: AM
authors: Müller
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000378:metabolism*; D015820:Cadherins / Q000378:metabolism*; D002199:Capillary Permeability; D016022:Case-Control Studies; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D015536:Down-Regulation; D042783:Endothelial Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D005260:Female; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism; D006801:Humans; D007223:Infant; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D012128:Respiratory Distress Syndrome / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D018805:Sepsis / Q000150:complications* / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult; D000099152:Cadherin 5
chemical_list: D015703:Antigens, CD; D015820:Cadherins; D018836:Inflammation Mediators; D007371:Interferon-gamma; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D000099152:Cadherin 5