Abstract

BackgroundThe role of pro-inflammatory lipids in systemic immune activation in HIV infection remains largely unknown. We hypothesized that HIV-1-infected persons on antiretroviral therapy would have pro-inflammatory high density lipoprotein (HDL), and that an apoA-1 mimetic peptide might reverse the inflammatory properties of HDL in these persons.MethodsPlasma was obtained from 10 HIV-1-infected individuals on combination antiretroviral therapy with suppressed viremia and was incubated with the apoA-I mimetic peptide L-4F or sham-treated prior to isolation of HDL. The HDL that was isolated from each sample was tested for its ability to inhibit LDL-induced MCP-1 production in cultures of human aortic endothelial cells.ResultsWe found in a small pilot study of HIV-1-infected individuals with suppressed viremia on combination antiretroviral therapy that oxidative stress and inflammation in HIV-1 are associated with a marked reduction of HDL antioxidant/anti-inflammatory activities. In vitro, these abnormalities were significantly improved by treatment with the apoA-1 mimetic peptide, 4F.ConclusionsThese preliminary observations suggest that the anti-inflammatory properties of HDL are defective in HIV-1-infected persons despite treatment that is considered to be virologically successful.

Highlights

  • The role of pro-inflammatory lipids in systemic immune activation in HIV infection remains largely unknown

  • high density lipoprotein (HDL)-containing Fast protein liquid chromatography (FPLC) fractions were tested for their ability to inhibit low density lipoprotein (LDL)-induced Monocyte chemotactic protein1 (MCP-1) production in cultures of human aortic endothelial cells as previously described [9]

  • HDL inflammatory index (HII) is calculated from the ratio LDL-induced monocyte chemotactic activity in the presence of HDL/LDL-induced monocyte chemotactic activity in cultures of human aortic endothelial cells in the absence of HDL [9]

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Summary

Methods

Plasma was obtained from 10 HIV-1-infected individuals on combination antiretroviral therapy with suppressed viremia and was incubated with the apoA-I mimetic peptide L-4F or sham-treated prior to isolation of HDL. The HDL that was isolated from each sample was tested for its ability to inhibit LDL-induced MCP-1 production in cultures of human aortic endothelial cells

Results
Conclusions
Materials and methods
Discussion
Currier JS
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