Acute exposure to apolipoprotein A1 inhibits macrophage chemotaxis in vitro and monocyte recruitment in vivo

Research output: Contribution to journalArticlepeer-review


  • Tessa J Barrett
  • Lewis Taylor
  • Eileen McNeill
  • Arun Manmadhan
  • Carlota Recio
  • Alfredo Carmineri
  • Maximillian H Brodermann
  • Gemma E White
  • Dianne Cooper
  • Joseph A DiDonato
  • Maryam Zamanian-Daryoush
  • Stanley L Hazen
  • Keith M Channon
  • David R Greaves
  • Edward A Fisher

Colleges, School and Institutes

External organisations

  • University of Oxford
  • Marc and Ruti Bell Program in Vascular Biology, NYU School of Medicine, New York, United States.
  • Queen Mary University of London
  • Department of Cellular and Molecular Medicine, Lerner Research Institute of the Cleveland Clinic, Cleavland, United States.


Apolipoprotein A1 (apoA1) is the major protein component of high-density lipoprotein (HDL) and has well documented anti-inflammatory properties. To better understand the cellular and molecular basis of the anti-inflammatory actions of apoA1, we explored the effect of acute human apoA1 exposure on the migratory capacity of monocyte-derived cells in vitro and in vivo. Acute (20-60 min) apoA1 treatment induced a substantial (50-90%) reduction in macrophage chemotaxis to a range of chemoattractants. This acute treatment was anti-inflammatory in vivo as shown by pre-treatment of monocytes prior to adoptive transfer into an on-going murine peritonitis model. We find that apoA1 rapidly disrupts membrane lipid rafts, and as a consequence, dampens the PI3K/Akt signalling pathway that coordinates reorganization of the actin cytoskeleton and cell migration. Our data strengthen the evidence base for therapeutic apoA1 infusions in situations where reduced monocyte recruitment to sites of inflammation could have beneficial outcomes.


Original languageEnglish
Article numbere15190
Number of pages23
Publication statusPublished - 30 Aug 2016