title: Neutrophil activation status in stable coronary artery disease.
abstract: BACKGROUND
  During the last years, neutrophils have emerged as important players in atherogenesis. They are highly activated in peripheral blood of patients with unstable angina. Moreover, a primed state of circulating neutrophils has been proposed in patients with stable angina. Our aim was to investigate the neutrophil activation status in patients with stable coronary artery disease (CAD) at conventional drug treatment.
  
  
  RESULTS
  Thirty patients with stable CAD and 30 healthy controls were included using a paired design. The neutrophil expression of CD18 and high-affinity state of CD11b was analysed by flow cytometry before and after stimulation with chemoattractants. Also, the production of reactive oxygen species (ROS) was determined by chemiluminescence. During basal conditions, the neutrophil expression of CD18 or high-affinity state of CD11b did not differ between patients and controls. Chemoattractants (Interleukin-8 and Leukotriene B(4)) did not increase either the expression or the amount of high-affinity CD11b/CD18-integrins in CAD patients compared to controls, and had no effect on the production of ROS. On the other hand, the ROS production in response to C3bi-opsonised yeast particles and the neutrophils' inherent capacity to produce ROS were both significantly decreased in patients.
  
  
  CONCLUSIONS
  We could not find any evidence that neutrophils in patients with stable CAD were primed, i.e. more prone to activation, compared to cells from healthy controls. According to our data, the circulating neutrophils in CAD patients rather showed an impaired activation status. It remains to be elucidated whether the neutrophil dysfunction in CAD is mainly a marker of chronic disease, an atherogenic factor or a consequence of the drug treatment.
authors.affiliation: Division of Medical Microbiology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. eva.sarndahl@ikm.oru.se
authors.forename: Eva
authors.initials: E
authors.lastname: Särndahl
authors.forename: Ida
authors.initials: I
authors.lastname: Bergström
authors.forename: Veronika Patcha
authors.initials: VP
authors.lastname: Brodin
authors.forename: Johnny
authors.initials: J
authors.lastname: Nijm
authors.forename: Helen
authors.initials: H
authors.lastname: Lundqvist Setterud
authors.forename: Lena
authors.initials: L
authors.lastname: Jonasson
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000473:pathology; D050197:Atherosclerosis / Q000097:blood / Q000473:pathology; D039481:CD11b Antigen / Q000096:biosynthesis; D018821:CD18 Antigens / Q000096:biosynthesis; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D009504:Neutrophils / Q000378:metabolism; D017382:Reactive Oxygen Species; D015398:Signal Transduction
chemical_list: D039481:CD11b Antigen; D018821:CD18 Antigens; D017382:Reactive Oxygen Species