Effect of chronic Pseudomonas aeruginosa infection on the development of atherosclerosis in a rat model


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Turkay C., Saba R., Pahin N., Altunbap H., Ozbudak O., Akkaya B., ...Daha Fazla

CLINICAL MICROBIOLOGY AND INFECTION, cilt.10, sa.8, ss.705-708, 2004 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 10 Sayı: 8
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1111/j.1469-0691.2004.00920.x
  • Dergi Adı: CLINICAL MICROBIOLOGY AND INFECTION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.705-708
  • Anahtar Kelimeler: atherosclerosis, chronic infection, pathogenesis, Pseudomonas aeruginosa, rat model, CORONARY-ARTERY-DISEASE, CHLAMYDIA-PNEUMONIAE, AZITHROMYCIN, CHOLESTEROL, AGENTS, MOUSE
  • Akdeniz Üniversitesi Adresli: Evet

Özet

In order to investigate the possible relationship between atherosclerosis and chronic Pseudomonas aeruginosa infection, 66 Wistar rats were given five separate intratracheal inoculations of either P. aeruginosa or sterile saline at 4-week intervals. The rats were divided into four groups: group 1 was infected with P. aeruginosa and fed a diet containing cholesterol 1% w/v; group 2 was infected with P. aeruginosa and fed a normal diet; group 3 was not infected and was fed a diet containing cholesterol 1% w/v; and group 4 (the control group) was not infected and was fed a normal diet. One month after the final inoculation, the rats were killed humanely; computerised image analysis was used to evaluate sections of the aorta and heart, and the maximal wall thickness of the aorta and coronary artery. The aortic wall thickness was significantly greater for group 1 (329.53 +/- 58.06 mum) compared to groups 2 (190.59 +/- 27.81 mum; p < 0.0001), 3 (262.90 +/- 61.12 mu m; p < 0.0004) and 4 (158.00 +/- 30.30 mum; p < 0.0001). Similarly, the coronary artery wall thickness was significantly greater for group 1 (72.96 +/- 10.67 mu m) compared to groups 2 (35.07 +/- 8.53 mu m; p < 0.0001), 3 (41.45 +/- 10.22 mum; p < 0.0001) and 4 (32.30 +/- 5.27 mu m; p < 0.0001). These findings strengthen the hypothesis that chronic infection plays a role in the pathogenesis of atherosclerosis.