Linoleic acid increases monocyte deformation and adhesion to endothelium.

Published

Journal Article

Fatty acids have been implicated in having both anti- or pro-inflammatory actions, which may contribute to the progression and severity of atherosclerosis. Linoleic acid has been shown by others to decrease CD18 expression and leukocyte adhesion under static conditions. We investigated the effect of steric acid (18:0), oleic acid (18:1), and linoleic acid (18:2) on the cortical tension (a measure of cell membrane deformability) and adhesion characteristics of the monocytic cell line Mono Mac 6 (MM6) cells to TNF-alpha activated HUVEC under fluid flow. Linoleic acid concentrations up to 23 microM decreased cortical tension and increased adhesion frequencies. Increased adhesion was not due to altered cell morphology or adhesion kinetics and occurred despite decreases in receptor expression (CD18 and CD11a). At higher levels of linoleic acid (> or = 46 microM), cell dissociation constants significantly increased. Results show that decreasing cortical tension increased the probability that contact between MM6 cells and endothelium would produce an adhesive interaction, possibly due to increased deformation of the microvilli and the cell membrane cortex. However, more deformable cells rolled more erratically at low shear rates. The different behavior during initial contact and rolling suggest that adhesion is influenced by two force-dependent mechanisms, deformation of microvilli and a steric barrier. Incubation of MM6 with 23 microM steric or oleic acid did not significantly affect cortical tension. However, cells incubated with steric acid greatly increased their adherence to HUVEC and cells incubated with oleic acid showed no significant effect, indicating factors other than deformability may dominate.

Full Text

Duke Authors

Cited Authors

  • Rinker, KD; Kirkpatrick, AP; Ting-Beall, HP; Shepherd, RD; Levin, JD; Irick, J; Thomas, JL; Truskey, GA

Published Date

  • December 2004

Published In

Volume / Issue

  • 177 / 2

Start / End Page

  • 275 - 285

Pubmed Central ID

  • 15530900

Electronic International Standard Serial Number (EISSN)

  • 1879-1484

International Standard Serial Number (ISSN)

  • 0021-9150

Digital Object Identifier (DOI)

  • 10.1016/j.atherosclerosis.2004.07.017

Language

  • eng