title: Differential expression of prostaglandin E2 and interleukin-6 in occlusive and aneurysmal aortic disease.
abstract: BACKGROUND
  Both aortoiliac occlusive disease (AIOD) and abdominal aortic aneurysm disease (AAA) are traditionally considered degenerative conditions that are caused by atherosclerosis. Although it is becoming apparent that the pathophysiology of each condition has its own determinants, inflammation is thought to play a role in each. The purpose of this study was to analyze the inflammatory cytokines interleukin-6 (IL-6) and prostaglandin E2 (PGE2) in aortic disease and compare AAA with AIOD, as well as to compare both with normal aorta.
  
  
  METHODS
  Aortic tissue was harvested at the time of aortic reconstructive surgery for AAA (n = 13) and AIOD (n = 14) or at time of organ harvest for normal (n = 16) aortic specimens. Whole organ cultures were immediately established, and the culture medium was collected after 72 hours. An enzyme-linked immunosorbent assay was used to assay for PGE2 and a lymphoproliferative assay was used to quantitate IL-6. Statistical analysis was performed using paired 2-tail t tests.
  
  
  RESULTS
  Normal aorta expressed much less PGE2 (384 +/- 67 ng/mL) than either AAA (11,093 +/- 7,411 ng/mL) (P < .001) or AIOD (13, 719 +/- 3,355 ng/mL) (P < .002). However there was no statistically significant difference in PGE2 expression between the AAA and AIOD groups (P = . 44). The IL-6 assay also showed that normal aorta had very little expression (1,861 +/- 334 U/mL) compared with either AAA (14,329 +/- 4,159 U/mL) (P = . 02) or AIOD (39,805 +/- 8,426) (P < .001). Comparison between AAA and AIOD revealed significantly higher expression of IL-6 by the AIOD cultures (P = .03).
  
  
  CONCLUSIONS
  AAA and AIOD are associated with increased expression of the proinflammatory cytokines PGE2 and IL-6. However, AIOD is associated with a much higher level of IL-6 expression than is AAA, although the level of PGE2 expression is the same. This differential expression of IL-6 may help explain the pathogenesis of these 2 distinct aortic diseases.
authors.affiliation: Department of Surgery, Washington University School of Medicine, John Cochran Veterans Administration Medical Center, St Louis, MO, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Reilly
authors.forename: M
authors.initials: M
authors.lastname: Miralles
authors.forename: W N
authors.initials: WN
authors.lastname: Wester
authors.forename: G A
authors.initials: GA
authors.lastname: Sicard
mesh_terms: D001012:Aorta, Abdominal / Q000378:metabolism; D017544:Aortic Aneurysm, Abdominal / Q000378:metabolism*; D001157:Arterial Occlusive Diseases / Q000378:metabolism*; D001161:Arteriosclerosis / Q000378:metabolism; D015232:Dinoprostone / Q000096:biosynthesis*; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis*; D009924:Organ Culture Techniques
chemical_list: D015850:Interleukin-6; D015232:Dinoprostone