title: Transcriptional regulation of alpha5beta1 integrin, fibronectin, VCAM-1, MCSF-1/c-fms, and MCP-1 in atrioventricular valves after valvular surgery and Staphylococcus aureus bacteremia.
abstract: OBJECTIVE
  The primary event in the development of infective endocarditis (IE) is bacterial adherence to damaged heart valves. This includes capture, adhesion and internalization of bacteria into host cells.
  
  
  METHODS
  We determined in an experimental rabbit model for IE whether a transient bacteremia caused by Staphylococcus aureus and/or endothelial heart valve lesions induce transcriptional regulation of alpha(5)beta(1) integrin, fibronectin, vascular cell adhesion molecule-1 (VCAM-1), macrophage colony-stimulating factor-1 (MCSF-1), c-fms proto-oncogene (MCSF-1 receptor), and macrophage chemoattractant protein-1 (MCP-1) in mitral and tricuspid valves.
  
  
  RESULTS
  No significant upregulation was found after isolated bacteremia. Six hours after surgical manipulation valvular endothelial lesions led to a distinct modulation in the mRNA expression of proinflammatory cytokines (MCSF-1 and MCP-1), VCAM-1 and alpha(5)beta(1) integrin. The most evident differences between the mitral and tricuspid valves were seen in the significant upregulation of VCAM-1 mRNA on the tricuspid valve in the surgical groups, whereas there was no effect on the mitral valve. MCSF-1 and MCP-1 were dramatically upregulated in both valves after surgery.
  
  
  CONCLUSIONS
  During the host defence mechanisms in the development of IE proinflammatory cytokines, cellular adhesion molecules, and molecules of the fibronectin/integrin axis are activated, showing distinct differences in right- and left-sided heart valves.
authors.affiliation: German Heart Center Munich at the Technical University of Munich, Department of Cardiac and Vascular Surgery, Germany.
authors.forename: Walter Benno
authors.initials: WB
authors.lastname: Eichinger
authors.forename: Joachim Burkhard
authors.initials: JB
authors.lastname: Grammer
authors.forename: Bo
authors.initials: B
authors.lastname: Zhao
authors.forename: Juliane
authors.initials: J
authors.lastname: Brückner
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Mendler
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Lange
authors.forename: Robert
authors.initials: R
authors.lastname: Bauernschmitt
mesh_terms: D000818:Animals; D016470:Bacteremia / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology; D001422:Bacterial Adhesion; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D018932:Chemokine CCL2 / Q000235:genetics; D004195:Disease Models, Animal; D005353:Fibronectins / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D006350:Heart Valve Prosthesis; D016023:Integrins / Q000235:genetics / Q000378:metabolism; D016173:Macrophage Colony-Stimulating Factor / Q000235:genetics / Q000378:metabolism; D008943:Mitral Valve / Q000601:surgery*; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013203:Staphylococcal Infections / Q000235:genetics / Q000378:metabolism*; D013211:Staphylococcus aureus / Q000235:genetics; D014158:Transcription, Genetic; D014261:Tricuspid Valve / Q000601:surgery*; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D018932:Chemokine CCL2; D005353:Fibronectins; D016023:Integrins; D012333:RNA, Messenger; D019010:Vascular Cell Adhesion Molecule-1; D016173:Macrophage Colony-Stimulating Factor