4.4 Article

Monocyte activation in persons living with HIV and tuberculosis coinfection

期刊

AIDS
卷 35, 期 3, 页码 447-452

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QAD.0000000000002766

关键词

HIV; immune activation; inflammation; monocyte; tuberculosis

资金

  1. National Center for Advancing Translational Science at the National Institutes of Health [KL2 TR001426]
  2. National Heart, Lung, and Blood Institute at the National Institutes of Health [K23 HL123341]
  3. National Institute of Allergy and Infectious Diseases at the National Institutes of Health [UM1AI069501, UM1 AI068636]
  4. Faculty Pilot Award from the Department of Internal Medicine at the University of Cincinnati College of Medicine

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The study found that in HIV-infected individuals with LTBI or prior active TB, there was enhanced monocyte activation, which may contribute to the pathogenesis of noncommunicable diseases.
Objectives: To characterize monocyte subsets and activation in persons living with HIV (PLWH) with tuberculosis coinfection. Design: Cross-sectional study within a cohort of PLWH and HIV-uninfected participants at the Joint Clinical Research Centre in Kampala, Uganda. Methods: Participants were at least 45 years old with at least one cardiovascular risk factor. PLWH had an HIV viral load 1000 copies/ml or less on stable antiretroviral therapy prior to cohort entry. QuantiFERON-TB testing was performed to define latent tuberculosis infection (LTBI). Prior active TB was defined by self-report and verified by medical records. Blood was stained with monocyte subset markers (CD14(+), CD16), CD62p, CD69, CX3CR1, HLA-DR, and tissue factor, and examined with flow cytometry. Results: One hundred and twenty-five participants (83 PLWH and 42 without HIV) were included. Median CD4(+) count was 582 cells/mu l in PLWH. PLWH had a higher frequency of total monocytes (4.3% vs. 3.2%; P < 0.001) and inflammatory monocyte subset (15.5% vs. 11.7%; P = 0.016) compared with HIV-uninfected individuals. No differences in the frequency of monocyte subsets were observed by TB status. Among PLWH, prior active TB was associated with increased frequency of total monocytes compared with LTBI (5.1% vs. 3.7%; P = 0.013). HLA-DR density on monocytes was three-fold higher in PLWH with LTBI or prior TB compared with PLWH without LTBI (P = 0.002). In multivariate analysis, a higher monocyte HLA-DR density remained associated with LTBI or prior TB in PLWH (log-MFI; b = 1.17; P < 0.001). Conclusion: Our findings indicate enhanced monocyte activation in PLWH with LTBI or prior active TB, which may contribute to the pathogenesis of noncommunicable diseases in HIV.

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