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Plasma sphingolipids in HIV-associated chronic obstructive pulmonary disease
Shane Hodgson1, Timothy J Griffin2, Cavan Reilly3
1Department of Medicine, University of Minnesota, Minneapolis, Minnesota, USA.
BMJ Open Respiratory Research
|April 15, 2017
Summary
HIV-associated COPD has a unique metabolite profile, including sphingolipids. Tryptophan metabolism is elevated in HIV but doesn't directly cause COPD in these patients.
Area of Science:
- Metabolomics
- HIV research
- Pulmonary medicine
Background:
- Chronic obstructive pulmonary disease (COPD) is a significant comorbidity in people living with HIV (PLWH).
- HIV infection may uniquely contribute to COPD development, independent of smoking.
- The underlying mechanisms of HIV-associated COPD (HIV-COPD) remain unclear.
Purpose of the Study:
- To identify metabolomic biomarkers for HIV-COPD.
- To elucidate potential mechanistic pathways involved in HIV-COPD.
Main Methods:
- Case-control study involving plasma metabolite profiling using mass spectrometry.
- Comparison of 38 individuals with HIV-COPD against matched controls.
- Untargeted and targeted metabolomics, including liquid chromatography with mass spectrometry (LC-MS/MS) for tryptophan (Trp) and kynurenine (Kyn) analysis.
Main Results:
- 1689 analytes were associated with HIV-COPD (10% false discovery rate).
- 263 analytes differed between PLWH with and without COPD.
- Elevated kynurenine/tryptophan ratio observed in PLWH, but not significantly linked to COPD status.
Conclusions:
- HIV-COPD exhibits a distinct metabolomic signature, characterized by specific sphingolipids.
- While tryptophan metabolism is altered in HIV, it does not appear to be a direct driver of COPD in this population.