title: Multiple bacteria contribute to intraplaque T-cell activation in atherosclerosis.
abstract: BACKGROUND
  Infection with microorganisms is considered a pathogenic factor in atherogenesis. Several studies have shown the presence of a broad spectrum of bacterial species in atherosclerotic plaques, which could trigger local inflammation. Because T cells contribute to atherosclerotic plaque inflammation, we studied the responsiveness of human plaque derived T-cell cultures to bacteria of different species.
  
  
  METHODS
  Primary polyclonal T-cell cultures were generated from both carotid endarterectomy tissue and peripheral blood of nine patients, and the peripheral blood of eight matched controls. The in vitro proliferative responses of the T-cell cultures against H. pylori, N. meningitidis, N. lactamica, S. aureus, S. pneumoniae, S. epidermidis and E. coli were analysed. T-cell proliferation was measured by (3)H-thymidine incorporation and expressed as a stimulation index. Selective outgrowth of intraplaque microbial specific T cells was studied by calculating the ratio of plaque T-cell SI and peripheral blood T-cell SI in each patient.
  
  
  RESULTS
  All patients showed T-cell responsiveness to multiple bacteria in their plaque tissue. Stimulation indices were in the range of 0.3-30, and this degree of reactivity with the different species was heterogeneous among patients. Selective outgrowth (plaque/peripheral blood ratio) of T cells against multiple bacteria was observed in six out of nine patients.
  
  
  CONCLUSIONS
  T cells in atherosclerotic plaques have the capacity to selectively respond to antigens of a wide variety of microbial antigens. This supports the view that such mechanisms could contribute to the atherosclerotic inflammatory response.
authors.affiliation: Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: J J
authors.initials: JJ
authors.lastname: van der Meer
authors.forename: A C
authors.initials: AC
authors.lastname: van der Wal
authors.forename: P
authors.initials: P
authors.lastname: Teeling
authors.forename: M M
authors.initials: MM
authors.lastname: Idu
authors.forename: A
authors.initials: A
authors.lastname: van der Ende
authors.forename: O J
authors.initials: OJ
authors.lastname: de Boer
mesh_terms: D000368:Aged; D000942:Antigens, Bacterial / Q000276:immunology*; D050197:Atherosclerosis / Q000276:immunology / Q000473:pathology*; D049109:Cell Proliferation; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013601:T-Lymphocytes / Q000382:microbiology / Q000473:pathology*
chemical_list: D000942:Antigens, Bacterial