Tiffany R Butterfield1, David B Hanna, Robert C Kaplan, Jorge R Kizer, Helen G Durkin, Mary A Young, Marek J Nowicki, Phyllis C Tien, Elizabeth T Golub, Michelle A Floris-Moore, Kehmia Titanji, Margaret A Fischl, Sonya L Heath, Jefferey Martinson, Suzanne M Crowe, Clovis S Palmer, Alan L Landay, Joshua J Anzinger. 1. aDepartment of Microbiology, University of the West Indies, Mona, Kingston, Jamaica bDepartment of Epidemiology and Population Health cDepartment of Medicine, Albert Einstein College of Medicine, Bronx, New York dDepartment of Pathology, SUNY Downstate Medical Center, New York City, New York eDivision of Infectious Diseases, Georgetown University, Washington, D.C fDepartment of Medicine, University of Southern California, Los Angeles gDepartment of Medicine, University of California, San Francisco, California hDepartment of Epidemiology, Johns Hopkins University, Baltimore, Maryland iDivision of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina jDepartment of Medicine, Emory University, Atlanta, Georgia kDivision of Infectious Diseases, University of Miami Miller School of Medicine, Miami, Florida lDivision of Infectious Diseases, University of Alabama at Birmingham, Birmingham, Alabama mDepartment of Immunology and Microbiology, Rush University Medical Center, Chicago, Illinois, USA nCentre for Biomedical Research, Burnet Institute oDepartment of Infectious Diseases, Monash University pDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia.
Abstract
OBJECTIVE: People living with HIV (PLWH) have chronic immune activation and increased cardiovascular disease (CVD) risk. Activation of monocytes and T lymphocytes causes upregulation of glucose transporter-1 (GLUT1) for efficient function. PLWH have an increased percentage of GLUT1-expressing monocytes and T lymphocytes, but it is unclear if these cells are associated with CVD. We evaluated the expression of GLUT1 and CD38 on monocyte and T lymphocyte populations from HIV-infected women with subclinical CVD. METHODS: Participants with more than 75th percentile (n = 15) and less than 25th percentile (n = 15) age-adjusted intima-media thickness (IMT) at the right common carotid artery and bifurcation were identified from the Women's Interagency HIV Study. Groups were matched by age, race/ethnicity, smoking status, and CD4 cell count. All women were receiving suppressive antiretroviral therapy except for one high and one low IMT participant. Monocyte and T lymphocyte populations were evaluated for GLUT1 and CD38 expression using flow cytometry. RESULTS: Intermediate monocytes from high IMT women had significantly increased expression of GLUT1 (310 MFI vs. 210 MFI, P = 0.024) (66.4% vs. 48.5%, P = 0.031) and CD38 (339 MFI vs. 211 MFI, P = 0.002) (10.5% vs. 3.8%, P = 0.0002) compared with women with low IMT. High and low IMT participants showed no differences in GLUT1 or CD38 expression on classical monocytes, nonclassical monocytes, CD4 and CD8 T lymphocytes. CONCLUSION: GLUT1-expressing intermediate monocytes are elevated in HIV-infected women with subclinical CVD. These cells may contribute to development of CVD in PLWH and could be a novel target to limit inflammation.
OBJECTIVE: People living with HIV (PLWH) have chronic immune activation and increased cardiovascular disease (CVD) risk. Activation of monocytes and T lymphocytes causes upregulation of glucose transporter-1 (GLUT1) for efficient function. PLWH have an increased percentage of GLUT1-expressing monocytes and T lymphocytes, but it is unclear if these cells are associated with CVD. We evaluated the expression of GLUT1 and CD38 on monocyte and T lymphocyte populations from HIV-infected women with subclinical CVD. METHODS: Participants with more than 75th percentile (n = 15) and less than 25th percentile (n = 15) age-adjusted intima-media thickness (IMT) at the right common carotid artery and bifurcation were identified from the Women's Interagency HIV Study. Groups were matched by age, race/ethnicity, smoking status, and CD4 cell count. All women were receiving suppressive antiretroviral therapy except for one high and one low IMT participant. Monocyte and T lymphocyte populations were evaluated for GLUT1 and CD38 expression using flow cytometry. RESULTS: Intermediate monocytes from high IMT women had significantly increased expression of GLUT1 (310 MFI vs. 210 MFI, P = 0.024) (66.4% vs. 48.5%, P = 0.031) and CD38 (339 MFI vs. 211 MFI, P = 0.002) (10.5% vs. 3.8%, P = 0.0002) compared with women with low IMT. High and low IMT participants showed no differences in GLUT1 or CD38 expression on classical monocytes, nonclassical monocytes, CD4 and CD8 T lymphocytes. CONCLUSION: GLUT1-expressing intermediate monocytes are elevated in HIV-infected women with subclinical CVD. These cells may contribute to development of CVD in PLWH and could be a novel target to limit inflammation.
Authors: A Funaro; G C Spagnoli; C M Ausiello; M Alessio; S Roggero; D Delia; M Zaccolo; F Malavasi Journal: J Immunol Date: 1990-10-15 Impact factor: 5.422
Authors: H N Hodis; W J Mack; R A Lobo; D Shoupe; A Sevanian; P R Mahrer; R H Selzer; C R Liu Cr; C H Liu Ch; S P Azen Journal: Ann Intern Med Date: 2001-12-04 Impact factor: 25.391
Authors: Kyrill S Rogacev; Sarah Seiler; Adam M Zawada; Birgit Reichart; Esther Herath; Daniel Roth; Christof Ulrich; Danilo Fliser; Gunnar H Heine Journal: Eur Heart J Date: 2010-10-12 Impact factor: 29.983
Authors: Joshua J Anzinger; Tiffany R Butterfield; Thomas A Angelovich; Suzanne M Crowe; Clovis S Palmer Journal: J Immunol Res Date: 2014-06-12 Impact factor: 4.818
Authors: Melissa E Schechter; Bruno B Andrade; Tianyu He; George Haret Richter; Kevin W Tosh; Benjamin B Policicchio; Amrit Singh; Kevin D Raehtz; Virginia Sheikh; Dongying Ma; Egidio Brocca-Cofano; Cristian Apetrei; Russel Tracy; Ruy M Ribeiro; Alan Sher; Ivo M B Francischetti; Ivona Pandrea; Irini Sereti Journal: Sci Transl Med Date: 2017-08-30 Impact factor: 17.956
Authors: Hui-Ling Yeoh; Allen C Cheng; Catherine L Cherry; Jacquelyn M Weir; Peter J Meikle; Jennifer F Hoy; Suzanne M Crowe; Clovis S Palmer Journal: EBioMedicine Date: 2017-07-18 Impact factor: 8.143
Authors: Hesham M Shehata; Andrew J Murphy; Man Kit Sam Lee; Clair M Gardiner; Suzanne M Crowe; Shomyseh Sanjabi; David K Finlay; Clovis Steve Palmer Journal: Front Immunol Date: 2017-10-16 Impact factor: 7.561
Authors: Jehad Alzahrani; Tabinda Hussain; David Simar; Riya Palchaudhuri; Mohamed Abdel-Mohsen; Suzanne M Crowe; George W Mbogo; Clovis S Palmer Journal: EBioMedicine Date: 2019-07-18 Impact factor: 8.143
Authors: Corrilynn O Hileman; Robert C Kalayjian; Sausan Azzam; Daniela Schlatzer; Kunling Wu; Katherine Tassiopoulos; Roger Bedimo; Ronald J Ellis; Kristine M Erlandson; Asha Kallianpur; Susan L Koletar; Alan L Landay; Frank J Palella; Babafemi Taiwo; Muralidhar Pallaki; Charles L Hoppel Journal: Clin Infect Dis Date: 2021-08-02 Impact factor: 20.999
Authors: Maia Kavanagh Williamson; Naomi Coombes; Florian Juszczak; Marios Athanasopoulos; Mariam B Khan; Thomas R Eykyn; Ushani Srenathan; Leonie S Taams; Julianna Dias Zeidler; Andrea T Da Poian; Hendrik Huthoff Journal: Viruses Date: 2018-03-07 Impact factor: 5.048