Gut microbial-related choline metabolite trimethylamine-N-oxide is associated with progression of carotid artery atherosclerosis in HIV infection

Zhilei Shan; Clary B. Clish; Simin Hua; Justin M. Scott; David B. Hanna; Robert D. Burk; Sabina A. Haberlen; Sanjiv J. Shah; Joseph B. Margolick; Cynthia L. Sears; Wendy S. Post; Alan L. Landay; Jason M. Lazar; Howard N. Hodis; Kathryn Anastos; Robert C. Kaplan; Qibin Qi

doi:10.1093/infdis/jiy356

Gut microbial-related choline metabolite trimethylamine-N-oxide is associated with progression of carotid artery atherosclerosis in HIV infection

Zhilei Shan, Clary B. Clish, Simin Hua, Justin M. Scott, David B. Hanna, Robert D. Burk, Sabina A. Haberlen, Sanjiv J. Shah, Joseph B. Margolick, Cynthia L. Sears, Wendy S. Post, Alan L. Landay, Jason M. Lazar, Howard N. Hodis, Kathryn Anastos, Robert C. Kaplan, Qibin Qi^*

^*Corresponding author for this work

Medicine, Cardiology Division

Research output: Contribution to journal › Article › peer-review

39 Scopus citations

Abstract

We examined associations of 5 plasma choline metabolites with carotid plaque among 520 HIV-infected and 217 HIV-uninfected participants (112 incident plaque cases) over 7 years. After multivariable adjustment, higher gut microbiota-related metabolite trimethylamine-N-oxide (TMAO) was associated with an increased risk of carotid plaque in HIV-infected participants (risk ratio = 1.25 per standard deviation increment; 95% confidence interval, 1.05-1.50; P = .01). TMAO was positively correlated with biomarkers of monocyte activation and inflammation (sCD14, sCD163). Further adjustment for these biomarkers attenuated the association between TMAO and carotid plaque (P = .08). Among HIV-infected individuals, plasma TMAO was associated with carotid atherosclerosis progression, partially through immune activation and inflammation.

Original language	English (US)
Pages (from-to)	1474-1479
Number of pages	6
Journal	Journal of Infectious Diseases
Volume	218
Issue number	9
DOIs	https://doi.org/10.1093/infdis/jiy356
State	Published - Sep 22 2018

Funding

This work was supported by the National Heart, Lung, and Blood Institute (grant numbers K01HL129892 and R01HL140976 to Q. Q.; R01 HL126543, R01 HL132794, R01HL083760, R01HL095140 to R. C. K.; R01HL095129 to W. S. P.; and K01HL137557 to D. B. H.); and Feldstein Medical Foundation research grant to Q. Q. The WIHS is supported by the National Institute of Allergy and Infectious Diseases (NIAID), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Cancer Institute (NCI), the National Institute on Drug Abuse, and the National Institute on Mental Health. Targeted supplemental funding is also provided by the National Institute of Dental and Craniofacial Research, the National Institute on Alcohol Abuse and Alcoholism, the National Institute on Deafness and other Communication Disorders, and the NIH Office of Research on Women's Health. WIHS data collection is also supported by University of Southern California Clinical and Translational Science Award (grant number UL1-TR000004), Atlanta Clinical and Translational Science Award (grant number UL1-TR000454), and University of North Carolina Center for AIDS Research (grant number P30-AI-050410). The MACS is supported by the NIAID and NCI. MACS data collection is also supported by Johns Hopkins University Clinical and Translational Science Award (grant number UL1-TR000424). Financial support. This work was supported by the National Heart, Lung, and Blood Institute (grant numbers K01HL129892 and R01HL140976 to Q. Q.; R01 HL126543, R01 HL132794, R01HL083760, R01HL095140 to R. C. K.; R01HL095129 to W. S. P.; and K01HL137557 to D. B. H.); and Feldstein Medical Foundation research grant to Q. Q. The WIHS is supported by the National Institute of Allergy and Infectious Diseases (NIAID), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Cancer Institute (NCI), the National Institute on Drug Abuse, and the National Institute on Mental Health. Targeted supplemental funding is also provided by the National Institute of Dental and Craniofacial Research, the National Institute on Alcohol Abuse and Alcoholism, the National Institute on Deafness and other Communication Disorders, and the NIH Office of Research on Women’s Health. WIHS data collection is also supported by University of Southern California Clinical and Translational Science Award (grant number UL1-TR000004), Atlanta Clinical and Translational Science Award (grant number UL1-TR000454), and University of North Carolina Center for AIDS Research (grant number P30-AI-050410). The MACS is supported by the NIAID and NCI. MACS data collection is also supported by Johns Hopkins University Clinical and Translational Science Award (grant number UL1-TR000424).

Keywords

Carotid atherosclerosis
Choline metabolites
HIV infection
Risk factors
Trimethylamine-N-oxide

ASJC Scopus subject areas

General Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1093/infdis/jiy356

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Shan, Z., Clish, C. B., Hua, S., Scott, J. M., Hanna, D. B., Burk, R. D., Haberlen, S. A., Shah, S. J., Margolick, J. B., Sears, C. L., Post, W. S., Landay, A. L., Lazar, J. M., Hodis, H. N., Anastos, K., Kaplan, R. C., & Qi, Q. (2018). Gut microbial-related choline metabolite trimethylamine-N-oxide is associated with progression of carotid artery atherosclerosis in HIV infection. Journal of Infectious Diseases, 218(9), 1474-1479. https://doi.org/10.1093/infdis/jiy356

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title = "Gut microbial-related choline metabolite trimethylamine-N-oxide is associated with progression of carotid artery atherosclerosis in HIV infection",

abstract = "We examined associations of 5 plasma choline metabolites with carotid plaque among 520 HIV-infected and 217 HIV-uninfected participants (112 incident plaque cases) over 7 years. After multivariable adjustment, higher gut microbiota-related metabolite trimethylamine-N-oxide (TMAO) was associated with an increased risk of carotid plaque in HIV-infected participants (risk ratio = 1.25 per standard deviation increment; 95% confidence interval, 1.05-1.50; P = .01). TMAO was positively correlated with biomarkers of monocyte activation and inflammation (sCD14, sCD163). Further adjustment for these biomarkers attenuated the association between TMAO and carotid plaque (P = .08). Among HIV-infected individuals, plasma TMAO was associated with carotid atherosclerosis progression, partially through immune activation and inflammation.",

keywords = "Carotid atherosclerosis, Choline metabolites, HIV infection, Risk factors, Trimethylamine-N-oxide",

author = "Zhilei Shan and Clish, {Clary B.} and Simin Hua and Scott, {Justin M.} and Hanna, {David B.} and Burk, {Robert D.} and Haberlen, {Sabina A.} and Shah, {Sanjiv J.} and Margolick, {Joseph B.} and Sears, {Cynthia L.} and Post, {Wendy S.} and Landay, {Alan L.} and Lazar, {Jason M.} and Hodis, {Howard N.} and Kathryn Anastos and Kaplan, {Robert C.} and Qibin Qi",

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Shan, Z, Clish, CB, Hua, S, Scott, JM, Hanna, DB, Burk, RD, Haberlen, SA, Shah, SJ, Margolick, JB, Sears, CL, Post, WS, Landay, AL, Lazar, JM, Hodis, HN, Anastos, K, Kaplan, RC & Qi, Q 2018, 'Gut microbial-related choline metabolite trimethylamine-N-oxide is associated with progression of carotid artery atherosclerosis in HIV infection', Journal of Infectious Diseases, vol. 218, no. 9, pp. 1474-1479. https://doi.org/10.1093/infdis/jiy356

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T1 - Gut microbial-related choline metabolite trimethylamine-N-oxide is associated with progression of carotid artery atherosclerosis in HIV infection

AU - Shan, Zhilei

AU - Clish, Clary B.

AU - Hua, Simin

AU - Scott, Justin M.

AU - Hanna, David B.

AU - Burk, Robert D.

AU - Haberlen, Sabina A.

AU - Shah, Sanjiv J.

AU - Margolick, Joseph B.

AU - Sears, Cynthia L.

AU - Post, Wendy S.

AU - Landay, Alan L.

AU - Lazar, Jason M.

AU - Hodis, Howard N.

AU - Anastos, Kathryn

AU - Kaplan, Robert C.

AU - Qi, Qibin

PY - 2018/9/22

Y1 - 2018/9/22

N2 - We examined associations of 5 plasma choline metabolites with carotid plaque among 520 HIV-infected and 217 HIV-uninfected participants (112 incident plaque cases) over 7 years. After multivariable adjustment, higher gut microbiota-related metabolite trimethylamine-N-oxide (TMAO) was associated with an increased risk of carotid plaque in HIV-infected participants (risk ratio = 1.25 per standard deviation increment; 95% confidence interval, 1.05-1.50; P = .01). TMAO was positively correlated with biomarkers of monocyte activation and inflammation (sCD14, sCD163). Further adjustment for these biomarkers attenuated the association between TMAO and carotid plaque (P = .08). Among HIV-infected individuals, plasma TMAO was associated with carotid atherosclerosis progression, partially through immune activation and inflammation.

AB - We examined associations of 5 plasma choline metabolites with carotid plaque among 520 HIV-infected and 217 HIV-uninfected participants (112 incident plaque cases) over 7 years. After multivariable adjustment, higher gut microbiota-related metabolite trimethylamine-N-oxide (TMAO) was associated with an increased risk of carotid plaque in HIV-infected participants (risk ratio = 1.25 per standard deviation increment; 95% confidence interval, 1.05-1.50; P = .01). TMAO was positively correlated with biomarkers of monocyte activation and inflammation (sCD14, sCD163). Further adjustment for these biomarkers attenuated the association between TMAO and carotid plaque (P = .08). Among HIV-infected individuals, plasma TMAO was associated with carotid atherosclerosis progression, partially through immune activation and inflammation.

KW - Carotid atherosclerosis

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KW - HIV infection

KW - Risk factors

KW - Trimethylamine-N-oxide

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Gut microbial-related choline metabolite trimethylamine-N-oxide is associated with progression of carotid artery atherosclerosis in HIV infection

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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