Monocyte activation in persons living with HIV and tuberculosis coinfection.
Journal
AIDS (London, England)
ISSN: 1473-5571
Titre abrégé: AIDS
Pays: England
ID NLM: 8710219
Informations de publication
Date de publication:
01 03 2021
01 03 2021
Historique:
pubmed:
1
12
2020
medline:
28
4
2021
entrez:
30
11
2020
Statut:
ppublish
Résumé
To characterize monocyte subsets and activation in persons living with HIV (PLWH) with tuberculosis coinfection. Cross-sectional study within a cohort of PLWH and HIV-uninfected participants at the Joint Clinical Research Centre in Kampala, Uganda. 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. One hundred and twenty-five participants (83 PLWH and 42 without HIV) were included. Median CD4+ count was 582 cells/μl 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). 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.
Identifiants
pubmed: 33252496
pii: 00002030-202103010-00011
doi: 10.1097/QAD.0000000000002766
pmc: PMC7855758
mid: NIHMS1656545
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
447-452Subventions
Organisme : NIAID NIH HHS
ID : UM1 AI069501
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI069501
Pays : United States
Organisme : NIAID NIH HHS
ID : UM1 AI068636
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL123341
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR001426
Pays : United States
Informations de copyright
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
Références
Patel P, Rose CE, Collins PY, Nuche-Berenguer B, Sahasrabuddhe VV, Peprah E, et al. NIH HIV/NCD Project Disease Condition Technical Operating Group. Noncommunicable diseases among HIV-infected persons in low-income and middle-income countries: a systematic review and meta-analysis . AIDS 2018; 32: (Suppl 1): S5–S20.
Wong C, Gange SJ, Moore RD, Justice AC, Buchacz K, Abraham AG, et al. North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD). Multimorbidity among persons living with human immunodeficiency virus in the United States . Clin Infect Dis 2018; 66:1230–1238.
Deeks SG. HIV infection, inflammation, immunosenescence, and aging . Annu Rev Med 2011; 62:141–155.
Sullivan ZA, Wong EB, Ndung’u T, Kasprowicz VO, Bishai WR. Latent and active tuberculosis infection increase immune activation in individuals co-infected with HIV . EBioMedicine 2015; 2:334–340.
McCausland MR, Juchnowski SM, Zidar DA, Kuritzkes DR, Andrade A, Sieg SF, et al. Altered monocyte phenotype in HIV-1 infection tends to normalize with integrase-inhibitor-based antiretroviral therapy . PLoS One 2015; 10:e0139474.
Funderburg NT, Zidar DA, Shive C, Lioi A, Mudd J, Musselwhite LW, et al. Shared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome . Blood 2012; 120:4599–4608.
Ziegler-Heitbrock L, Ancuta P, Crowe S, Dalod M, Grau V, Hart DN, et al. Nomenclature of monocytes and dendritic cells in blood . Blood 2010; 116:e74–e80.
Thomas GD, Hamers AAJ, Nakao C, Marcovecchio P, Taylor AM, McSkimming C, et al. Human blood monocyte subsets: a new gating strategy defined using cell surface markers identified by mass cytometry . Arterioscler Thromb Vasc Biol 2017; 37:1548–1558.
Ziegler-Heitbrock L. The CD14+ CD16+ blood monocytes: their role in infection and inflammation . J Leukoc Biol 2007; 81:584–592.
Narasimhan PB, Marcovecchio P, Hamers AAJ, Hedrick CC. Nonclassical monocytes in health and disease . Annu Rev Immunol 2019; 37:439–456.
Cros J, Cagnard N, Woollard K, Patey N, Zhang SY, Senechal B, et al. Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors . Immunity 2010; 33:375–386.
Harris PA, Taylor R, Minor BL, Elliott V, Fernandez M, O’Neal L, et al. The REDCap consortium: building an international community of software platform partners . J Biomed Inform 2019; 95:103208.
Harris PA, Taylor R, Thielke R, Payne J, Gonzalez N, Conde JG. Research electronic data capture (REDCap)--a metadata-driven methodology and workflow process for providing translational research informatics support . J Biomed Inform 2009; 42:377–381.
Guo N, Chen Y, Su B, Yang X, Zhang Q, Song T, et al. Alterations of CCR2 and CX3CR1 on three monocyte subsets during HIV-1/Treponema pallidum Coinfection . Front Med (Lausanne) 2020; 7:272.
Krishnan S, Wilson EM, Sheikh V, Rupert A, Mendoza D, Yang J, et al. Evidence for innate immune system activation in HIV type 1-infected elite controllers . J Infect Dis 2014; 209:931–939.
McDevitt HO. Regulation of the immune response by the major histocompatibility system . N Engl J Med 1980; 303:1514–1517.
McLeish KR, Wellhausen SR, Dean WL. Biochemical basis of HLA-DR and CR3 modulation on human peripheral blood monocytes by lipopolysaccharide . Cell Immunol 1987; 108:242–248.
Gascon RL, Narvaez AB, Zhang R, Kahn JO, Hecht FM, Herndier BG, McGrath MS. Increased HLA-DR expression on peripheral blood monocytes in subsets of subjects with primary HIV infection is associated with elevated CD4 T-cell apoptosis and CD4 T-cell depletion . J Acquir Immune Defic Syndr 2002; 30:146–153.
Nemeth J, Olson GS, Rothchild AC, Jahn AN, Mai D, Duffy FJ, et al. Contained Mycobacterium tuberculosis infection induces concomitant and heterologous protection . PLoS Pathog 2020; 16:e1008655.
Huaman MA, Deepe J, George S, Fichtenbaum CJ. Elevated circulating concentrations of interferon-gamma in latent tuberculosis infection . Pathog Immun 2016; 1:291–303.
Huaman MA, Henson D, Rondan PL, Ticona E, Miranda G, Kryscio RJ, et al. Latent tuberculosis infection is associated with increased unstimulated levels of interferon-gamma in Lima, Peru . PLoS One 2018; 13:e0202191.
Kleinnijenhuis J, Quintin J, Preijers F, Joosten LA, Ifrim DC, Saeed S, et al. Bacille Calmette-Guerin induces NOD2-dependent nonspecific protection from reinfection via epigenetic reprogramming of monocytes . Proc Natl Acad Sci U S A 2012; 109:17537–17542.
Titanji B, Gavegnano C, Hsue P, Schinazi R, Marconi VC. Targeting inflammation to reduce atherosclerotic cardiovascular risk in people with HIV infection . J Am Heart Assoc 2020; 9:e014873.
Guaraldi G, Orlando G, Zona S, Menozzi M, Carli F, Garlassi E, et al. Premature age-related comorbidities among HIV-infected persons compared with the general population . Clin Infect Dis 2011; 53:1120–1126.
Pettit AC, Giganti MJ, Ingle SM, May MT, Shepherd BE, Gill MJ, et al. Antiretroviral Therapy Cohort Collaboration (ART-CC) investigators. Increased non-AIDS mortality among persons with AIDS-defining events after antiretroviral therapy initiation . J Int AIDS Soc 2018; 21:e25031.