title: Increased adhesiveness of isolated monocytes to endothelium is prevented by vitamin C intake in smokers.
abstract: BACKGROUND
  To explore pathophysiological mechanisms of cigarette smoking involved in atherogenesis, we compared adhesiveness of isolated blood monocytes with endothelium and plasma levels of the aqueous phase antioxidant vitamin C in nonsmokers and smokers before and after supplementation, using a novel monocyte adhesion assay with fixed human endothelial cells.
  
  
  RESULTS
  Monocyte adhesion to unstimulated human umbilical vein endothelial cells ranged from 0.17% to 0.51% in the nonsmoker group (0.37+/-0.09%, mean +/-SD, n=13). In smokers with a 1 to 2 packs per day consumption, monocyte adhesion was increased to 0.71+/-0.17% (mean +/-SD, n=10, P<.001), ranging from 0.46% to 0.99%. Increased adhesiveness was mediated by the integrin CD11b/CD18, as shown by inhibition with a monoclonal antibody to CD11b but not associated with altered CD11b surface expression. Plasma vitamin C levels were reduced in smokers (48.2+/-14.1 micromol/L) versus nonsmokers (67.7+/-17.6 micromol/L; P<.025), while no significant differences were found in retinol, vitamin E, or beta-carotene levels. This confirms that the radical scavenger vitamin C reacts sensitively to oxidative stress induced by cigarette smoke in human plasma. Consistently, dietary supplementation with vitamin C (2 g per day) for 10 days raised plasma levels to 82.6+/-11.0 micromol/L (n=10, P<.001) in smokers and decreased monocyte adhesion to values found in nonsmokers (0.38+/-0.18%, P<.001). In contrast, vitamin C intake did not affect monocyte adhesiveness in nonsmokers (0.37+/-0.14%, n=6) despite increasing plasma levels to 82.9+/-11.8 micromol/L.
  
  
  CONCLUSIONS
  Our data show that cigarette smoking increases CD11b-dependent monocyte adhesiveness in humans. Restoring reduced plasma vitamin C concentrations in smokers by oral supplementation decreased monocyte adhesion to values found in nonsmokers.
authors.affiliation: Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Ludwig-Maximilians-Universität, München, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Weber
authors.forename: W
authors.initials: W
authors.lastname: Erl
authors.forename: K
authors.initials: K
authors.lastname: Weber
authors.forename: P C
authors.initials: PC
authors.lastname: Weber
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D001161:Arteriosclerosis / Q000209:etiology* / Q000473:pathology; D001205:Ascorbic Acid / Q000502:physiology*; D002448:Cell Adhesion; D002478:Cells, Cultured; D004032:Diet; D004730:Endothelium, Vascular / Q000166:cytology*; D006801:Humans; D008297:Male; D009000:Monocytes / Q000166:cytology*; D010947:Plants, Toxic; D012907:Smoking; D014026:Nicotiana
chemical_list: D000975:Antioxidants; D001205:Ascorbic Acid