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Pro-inflammatory and pro-resolving lipid mediators of inflammation in HIV: effect of aspirin intervention

Jesmond Dalli1, Douglas Kitch2, Meagan P O'Brien3

  • 1William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK; Center for Inflammation and Therapeutic Innovation, Queen Mary University of London, London, UK.

Ebiomedicine
|February 15, 2023
PubMed

Insights

People with HIV (PWH) show altered lipid mediator profiles, with lower inflammation and higher pro-resolving mediators. Aspirin did not increase aspirin-triggered mediators in PWH, suggesting an impaired response.

Area of Science:

  • Lipid mediator biochemistry
  • Immunology of HIV infection
  • Cardiovascular disease risk factors

Background:

  • Persons with HIV (PWH) face higher cardiovascular disease (CVD) risk than HIV-seronegative (SN) individuals, partly due to inflammation.
  • The role of lipid mediators, key regulators of inflammation, in HIV infection is not well understood.
  • Aspirin, known to reduce CVD risk in the general population via anti-inflammatory lipid mediators, has not been studied in this context for PWH.

Purpose of the Study:

  • To investigate the relationship between plasma lipid mediators and HIV status.
  • To determine the impact of aspirin on lipid mediator profiles in PWH.

Main Methods:

  • Plasma samples from 110 PWH on antiretroviral therapy (ART) and 107 matched SN individuals were analyzed.
  • Quantification of 50 lipid mediators, including eicosanoids and specialized pro-resolving mediators (SPMs), was performed.
  • A randomized trial of aspirin (ACTG-A5331) data was used to assess aspirin's effects in PWH.

Main Results:

  • PWH exhibited lower levels of pro-inflammatory prostaglandins (PGs) and thromboxanes (Tx) but higher levels of certain pro-resolving lipid mediators (e.g., RvD4, MaR2n-3 DPA) compared to SN individuals.
  • Aspirin intervention in PWH reduced PGs and Tx levels.
  • Aspirin treatment did not increase aspirin-triggered mediators but led to the upregulation of other SPMs, such as MaR2n-3 DPA.

Conclusions:

  • Plasma lipid mediator profiles are altered in PWH, potentially influencing systemic inflammation and CVD risk.
  • Aspirin intervention in PWH did not elevate aspirin-triggered pro-resolving mediators.
  • These findings align with previous reports suggesting an impaired aspirin response in PWH.
Abstract

Keywords:
AspirinEicosanoidsHIVInflammationSPMs

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