title: Both cyclooxygenase- and cytokine-mediated inflammation are associated with carotid intima-media thickness.
abstract: BACKGROUND
  Common carotid artery intima-media thickness (CCA-IMT) is a valid index of atherosclerosis, which is viewed as an inflammatory disease. It is unknown if various modes of inflammation (cyclooxygenase [COX]-mediated, cytokine-mediated), oxidative stress and anti-oxidants are independently related to CCA-IMT.
  
  
  RESULTS
  We investigated cross-sectional relations between CCA-IMT measured by B-mode ultrasound and COX-mediated inflammation (as measured by 15-keto-dihydro-prostaglandin F(2alpha) [PGF(2alpha)], cytokine-mediated inflammation (interleukin-6 [IL-6], high sensitivity C-reactive protein [hsCRP] and serum amyloid A protein [SAA]), oxidative stress (8-iso-PGF(2alpha), an F(2)-isoprostane; a non-enzymatic, free radical-induced product of arachidonic acid), and tocopherols (anti-oxidants) in a small subset of a population-based sample of elderly men (n=234) stating no use of anti-inflammatory medications. In a backward-stepwise regression analysis of correlates of CCA-IMT (with PGF(2alpha), hsCRP, IL-6, SAA, F(2)-isoprostanes, tocopherols, diabetes, body mass index (BMI), beta-blocker, statin treatment, smoking, hypertension and cholesterol), PGF(2alpha), CRP, beta-blocker treatment, diabetes and BMI were independently associated with CCA-IMT. There were no associations between F(2)-isoprostanes or tocopherols and CCA-IMT in this study.
  
  
  CONCLUSIONS
  This study suggests both COX- and cytokine-mediated inflammation to be independently associated with increased CCA-IMT, implying that there might be more than one mode of inflammation involved in atherogenesis.
authors.affiliation: Department of Public Health and Caring Sciences/Geriatrics and Clinical Nutrition, Faculty of Medicine, Uppsala University, Uppsala Science Park, SE-751 85 Uppsala, Sweden. martin.wohlin@pubcare.uu.se
authors.forename: M
authors.initials: M
authors.lastname: Wohlin
authors.forename: J
authors.initials: J
authors.lastname: Helmersson
authors.forename: J
authors.initials: J
authors.lastname: Sundström
authors.forename: J
authors.initials: J
authors.lastname: Arnlöv
authors.forename: B
authors.initials: B
authors.lastname: Vessby
authors.forename: A
authors.initials: A
authors.lastname: Larsson
authors.forename: B
authors.initials: B
authors.lastname: Andrén
authors.forename: L
authors.initials: L
authors.lastname: Lind
authors.forename: S
authors.initials: S
authors.lastname: Basu
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000209:etiology; D002097:C-Reactive Protein / Q000378:metabolism; D017536:Carotid Artery, Common / Q000201:enzymology* / Q000276:immunology* / Q000473:pathology; D015331:Cohort Studies; D016207:Cytokines / Q000378:metabolism*; D015237:Dinoprost / Q000652:urine; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D008137:Longitudinal Studies; D008297:Male; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D000685:Serum Amyloid A Protein / Q000378:metabolism; D017539:Tunica Intima / Q000201:enzymology* / Q000276:immunology* / Q000473:pathology
chemical_list: D016207:Cytokines; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D000685:Serum Amyloid A Protein; D002097:C-Reactive Protein; D015237:Dinoprost; D011451:Prostaglandin-Endoperoxide Synthases