期刊
JOURNAL OF IMMUNOLOGY
卷 193, 期 11, 页码 5595-5603出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1303092
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资金
- Australian Centre for HIV and Hepatitis Virology Research
- University of Washington Center for AIDS Research
- National Institutes of Health [AI027757]
- National Institute of Allergy and Infectious Diseases
- National Cancer Institute
- National Institute of Mental Health
- National Institute on Drug Abuse
- National Institute of Child Health and Human Development
- National Heart, Lung, and Blood Institute
- National Institute on Aging
- Creative and Novel Ideas in HIV Research
- National Health and Medical Research Council of Australia Principal Research Fellowship
Monocyte activation during HIV-1 infection is associated with increased plasma levels of inflammatory markers and increased risk for premature development of age-related diseases. Because activated monocytes primarily use glucose to support cellular metabolism, we hypothesized that chronic monocyte activation during HIV-1 infection induces a hypermetabolic response with increased glucose uptake. To test this hypothesis, we evaluated glucose transporter 1 (Glut1) expression and glucose uptake by monocyte subpopulations in HIV-seropositive (HIV+) treatment-naive individuals (n = 17), HIV+ individuals on combination antiretroviral therapy with viral loads below detection (n = 11), and HIV-seronegative (HIV-) individuals (n = 16). Surface expression of Glut1 and cellular uptake of the fluorescent glucose analog 2-(N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2 deoxyglucose were analyzed by flow cytometry on monocyte subpopulations. Irrespective of treatment status, monocytes from HIV+ persons had significantly increased surface expression of Glut1 compared with those from HIV-controls. Nonclassical (CD14(+)CD16(++)) and intermediate (CD14(++) CD16(+)) monocyte subpopulations showed higher Glut1 expression than did classical (CD14(++)CD16(+)) monocytes. Intermediate monocytes from treatment-naive HIV+ individuals also showed increased uptake of 2-(N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2 deoxyglucose compared with those from HIV 2 controls. Our results show that HIV infection is associated with increased glucose metabolism in monocytes and that Glut1 expression by proinflammatory monocytes is a potential marker of inflammation in HIV-infected subjects. However, the possibility exists whereby other Gluts such as Glut3 and Glut4 may also support the influx of glucose into activated and inflammatory monocyte populations.
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