Influenza infection promotes macrophage traffic into arteries of mice that is prevented by D-4F, an apolipoprotein A-I mimetic peptide.

Academic Article


  • BACKGROUND: We reported that HDL loses its antiinflammatory properties during acute influenza A infection in mice, and we hypothesized that these changes might be associated with increased trafficking of macrophages into the artery wall. The present study tested this hypothesis. METHODS AND RESULTS: D-4F, an apolipoprotein A-I mimetic peptide, or vehicle in which it was dissolved (PBS) was administered daily to LDL receptor-null mice after a Western diet and after influenza infection. D-4F treatment increased plasma HDL cholesterol and paraoxonase activity compared with PBS and inhibited increases in LDL cholesterol and peak levels of interleukin-6 after infection. Lung viral titers were reduced by 50% in mice receiving D-4F. Injection of female mice with male macrophages, which were detected with real-time polymerase chain reaction to measure the male Sry gene, revealed a marked increase in macrophage traffic into the aortic arch and innominate arteries after infection that was prevented by administration of D-4F. CONCLUSIONS: We conclude that loss of antiinflammatory properties of HDL after influenza infection in mice is associated with increased arterial macrophage traffic that can be prevented by administration of D-4F.
  • Published In

  • Circulation  Journal
  • Keywords

  • Animals, Aorta, Thoracic, Apolipoprotein A-I, Aryldialkylphosphatase, Behavior, Animal, Body Temperature, Brachiocephalic Trunk, Cell Movement, Cells, Cultured, Diet, Atherogenic, Esterases, Female, Genes, sry, In Vitro Techniques, Interleukin-6, Lipoproteins, HDL, Lipoproteins, LDL, Macrophages, Peritoneal, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Monocytes, Orthomyxoviridae Infections, Peptides, Pneumonia, Receptors, LDL, T-Lymphocytes, Virus Replication
  • Author List

  • Van Lenten BJ; Wagner AC; Anantharamaiah GM; Garber DW; Fishbein MC; Adhikary L; Nayak DP; Hama S; Navab M; Fogelman AM
  • Start Page

  • 1127
  • End Page

  • 1132
  • Volume

  • 106
  • Issue

  • 9