Associations between surface markers on blood monocytes and carotid atherosclerosis in HIV-positive individuals

Clare Louise Westhorpe, Anna Maisa, Tim Denis Spelman, Jennifer F Hoy, Elizabeth M Dewar, Sofie Karapanagiotidis, Anna Hearps, Wan-Jung Cheng, Janine Maree Trevillyan, Sharon Ruth Lewin, Dimitri Sviridov, Julian Elliott, Anthony Jaworowski, Anthony M Dart, Suzanne Mary Crowe

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Abstract

Chronic HIV infection is associated with increased risk of cardiovascular disease (CVD), including in patients with virological suppression. Persistent innate immune activation may contribute to the development of CVD via activation of monocytes in these patients. We investigated whether changes in monocyte phenotype predict subclinical atherosclerosis in virologically suppressed HIV-positive individuals with low cardiovascular risk. We enroled 51 virologically suppressed HIV-positive individuals not receiving protease inhibitors or statins and 49 age-matched uninfected controls in this study. Carotid artery intima-media thickness (cIMT) was used as a surrogate marker for CVD, and traditional risk factors, including Framingham risk scores, were recorded. Markers of monocyte activation (CD14, CD16, CCR2, CX3CR1, CD38, HLA-DR and CD11b) were measured in whole-blood samples by flow cytometry. Associations were assessed using univariate and multivariate median regressions. Median cIMT was similar between HIV-positive and HIV-negative participants (P=0.3), although HIV-positive patients had significantly higher Framingham risk score (P=0.009) and systemic inflammation. Expression of two monocyte markers, CD11b and CX3CR1, independently predicted carotid artery thickness in HIV-positive individuals after controlling for Framingham risk score (P=0.025 and 0.015, respectively). These markers were not predictive of carotid artery thickening in controls. Our study indicates that monocyte surface markers may serve as novel predictors of CVD in HIV-positive individuals and is consistent with an important role for monocyte activation in the progression of HIV-related cardiovascular pathology.
Original languageEnglish
Pages (from-to)133 - 138
Number of pages6
JournalImmunology and Cell Biology
Volume92
Issue number2
DOIs
Publication statusPublished - 2014

Cite this

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title = "Associations between surface markers on blood monocytes and carotid atherosclerosis in HIV-positive individuals",
abstract = "Chronic HIV infection is associated with increased risk of cardiovascular disease (CVD), including in patients with virological suppression. Persistent innate immune activation may contribute to the development of CVD via activation of monocytes in these patients. We investigated whether changes in monocyte phenotype predict subclinical atherosclerosis in virologically suppressed HIV-positive individuals with low cardiovascular risk. We enroled 51 virologically suppressed HIV-positive individuals not receiving protease inhibitors or statins and 49 age-matched uninfected controls in this study. Carotid artery intima-media thickness (cIMT) was used as a surrogate marker for CVD, and traditional risk factors, including Framingham risk scores, were recorded. Markers of monocyte activation (CD14, CD16, CCR2, CX3CR1, CD38, HLA-DR and CD11b) were measured in whole-blood samples by flow cytometry. Associations were assessed using univariate and multivariate median regressions. Median cIMT was similar between HIV-positive and HIV-negative participants (P=0.3), although HIV-positive patients had significantly higher Framingham risk score (P=0.009) and systemic inflammation. Expression of two monocyte markers, CD11b and CX3CR1, independently predicted carotid artery thickness in HIV-positive individuals after controlling for Framingham risk score (P=0.025 and 0.015, respectively). These markers were not predictive of carotid artery thickening in controls. Our study indicates that monocyte surface markers may serve as novel predictors of CVD in HIV-positive individuals and is consistent with an important role for monocyte activation in the progression of HIV-related cardiovascular pathology.",
author = "Westhorpe, {Clare Louise} and Anna Maisa and Spelman, {Tim Denis} and Hoy, {Jennifer F} and Dewar, {Elizabeth M} and Sofie Karapanagiotidis and Anna Hearps and Wan-Jung Cheng and Trevillyan, {Janine Maree} and Lewin, {Sharon Ruth} and Dimitri Sviridov and Julian Elliott and Anthony Jaworowski and Dart, {Anthony M} and Crowe, {Suzanne Mary}",
year = "2014",
doi = "10.1038/icb.2013.84",
language = "English",
volume = "92",
pages = "133 -- 138",
journal = "Immunology and Cell Biology",
issn = "0818-9641",
publisher = "John Wiley & Sons",
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}

Associations between surface markers on blood monocytes and carotid atherosclerosis in HIV-positive individuals. / Westhorpe, Clare Louise; Maisa, Anna; Spelman, Tim Denis; Hoy, Jennifer F; Dewar, Elizabeth M; Karapanagiotidis, Sofie; Hearps, Anna; Cheng, Wan-Jung; Trevillyan, Janine Maree; Lewin, Sharon Ruth; Sviridov, Dimitri; Elliott, Julian; Jaworowski, Anthony; Dart, Anthony M; Crowe, Suzanne Mary.

In: Immunology and Cell Biology, Vol. 92, No. 2, 2014, p. 133 - 138.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Associations between surface markers on blood monocytes and carotid atherosclerosis in HIV-positive individuals

AU - Westhorpe, Clare Louise

AU - Maisa, Anna

AU - Spelman, Tim Denis

AU - Hoy, Jennifer F

AU - Dewar, Elizabeth M

AU - Karapanagiotidis, Sofie

AU - Hearps, Anna

AU - Cheng, Wan-Jung

AU - Trevillyan, Janine Maree

AU - Lewin, Sharon Ruth

AU - Sviridov, Dimitri

AU - Elliott, Julian

AU - Jaworowski, Anthony

AU - Dart, Anthony M

AU - Crowe, Suzanne Mary

PY - 2014

Y1 - 2014

N2 - Chronic HIV infection is associated with increased risk of cardiovascular disease (CVD), including in patients with virological suppression. Persistent innate immune activation may contribute to the development of CVD via activation of monocytes in these patients. We investigated whether changes in monocyte phenotype predict subclinical atherosclerosis in virologically suppressed HIV-positive individuals with low cardiovascular risk. We enroled 51 virologically suppressed HIV-positive individuals not receiving protease inhibitors or statins and 49 age-matched uninfected controls in this study. Carotid artery intima-media thickness (cIMT) was used as a surrogate marker for CVD, and traditional risk factors, including Framingham risk scores, were recorded. Markers of monocyte activation (CD14, CD16, CCR2, CX3CR1, CD38, HLA-DR and CD11b) were measured in whole-blood samples by flow cytometry. Associations were assessed using univariate and multivariate median regressions. Median cIMT was similar between HIV-positive and HIV-negative participants (P=0.3), although HIV-positive patients had significantly higher Framingham risk score (P=0.009) and systemic inflammation. Expression of two monocyte markers, CD11b and CX3CR1, independently predicted carotid artery thickness in HIV-positive individuals after controlling for Framingham risk score (P=0.025 and 0.015, respectively). These markers were not predictive of carotid artery thickening in controls. Our study indicates that monocyte surface markers may serve as novel predictors of CVD in HIV-positive individuals and is consistent with an important role for monocyte activation in the progression of HIV-related cardiovascular pathology.

AB - Chronic HIV infection is associated with increased risk of cardiovascular disease (CVD), including in patients with virological suppression. Persistent innate immune activation may contribute to the development of CVD via activation of monocytes in these patients. We investigated whether changes in monocyte phenotype predict subclinical atherosclerosis in virologically suppressed HIV-positive individuals with low cardiovascular risk. We enroled 51 virologically suppressed HIV-positive individuals not receiving protease inhibitors or statins and 49 age-matched uninfected controls in this study. Carotid artery intima-media thickness (cIMT) was used as a surrogate marker for CVD, and traditional risk factors, including Framingham risk scores, were recorded. Markers of monocyte activation (CD14, CD16, CCR2, CX3CR1, CD38, HLA-DR and CD11b) were measured in whole-blood samples by flow cytometry. Associations were assessed using univariate and multivariate median regressions. Median cIMT was similar between HIV-positive and HIV-negative participants (P=0.3), although HIV-positive patients had significantly higher Framingham risk score (P=0.009) and systemic inflammation. Expression of two monocyte markers, CD11b and CX3CR1, independently predicted carotid artery thickness in HIV-positive individuals after controlling for Framingham risk score (P=0.025 and 0.015, respectively). These markers were not predictive of carotid artery thickening in controls. Our study indicates that monocyte surface markers may serve as novel predictors of CVD in HIV-positive individuals and is consistent with an important role for monocyte activation in the progression of HIV-related cardiovascular pathology.

UR - http://www.nature.com/icb/journal/vaop/ncurrent/pdf/icb201384a.pdf

U2 - 10.1038/icb.2013.84

DO - 10.1038/icb.2013.84

M3 - Article

VL - 92

SP - 133

EP - 138

JO - Immunology and Cell Biology

JF - Immunology and Cell Biology

SN - 0818-9641

IS - 2

ER -