Infections and endothelial cell apoptosis

  • Dr Erkki Pesonen, Lund University Hospital, Sweden
  • Vet Malene Muusfeldt Birck, Faculty of Life Sciences, University of Copenhagen, Denmark
  • Dr Petru Liuba, Lund University Hospital, Sweden
  • Dr Michal Odermarsky, Sweden
  • Dr Kenneth Persson, Malmö University Hospital, Sweden
  • Vet Axel Kornerup Hansen, Faculty of Life Sciences, University of Copenhagen, Denmark
  • Dr Antti Saraste, Turku University Hospital, Finland
  • Objectives. Endothelial cells of coronary arteries undergo apoptosis in patients with coronary artery disease. Carotid artery ultrasound studies show that after acute infections intima media thickness is increased. The possible effects of infections on endothelial cell apoptosis and the presence of apoptosis in early life remain unknown. Methods. Chlamydia pneumonia was inoculated three times at three weeks intervals to half of 32 piglets starting at the age of 8 weeks. Half of the piglets received cholesterol feeding. Morphological studies were done at the age of 19 weeks. Right coronary arteries were carefully excised and trimmed for excess tissue. The vessels were cut perpendicular to the long axis and sectioned at 5-µm thickness. TUNEL-assay was based on nick end labelling and staining of internucleosomal DNA fragments that are the biochemical hallmark of apoptosis. The percentage of apoptotic endothelial cells from intact endothelial cells was calculated using light microscopy. Results. Endothelial apoptosis appeared in 0.13 % (SD 0.30 %) of endothelial cells of non-infected piglets but in 0.75 % (SD 0.62) of infected piglets (p <0.005, t-test). In piglets fed with normal diet apoptosis appeared in 1.1% but in those on cholesterol rich diet the prevalence of apoptosis was lower 0.43 % (SD 0.42). Conclusions. Infections amplify endothelial cell apoptosis. The finding supports the notion that infection has a pro-atherogenic effect particularly in early life. Hypercholesterolemic diet did not further stimulate apoptosis.