Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 225, Issue 2, Pages 295-305Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiab341
Keywords
HIV; immune activation; inflammation; menopause; soluble CD14; soluble CD163
Categories
Funding
- National Institute of Mental Health [R01MH095683]
- National Institute of Allergy and Infectious Diseases [K24AI134326]
- National Heart, Lung, and Blood Institute [R01HL148094]
- NHLBI [U01-HL146241, U01-HL146201, U01-HL146204, U01-HL146202, U01-HL146193, U01-HL146245, U01-HL146240, U01-HL146242, U01-HL146333, U01-HL146205, U01-HL146203, U01-HL146208, U01-HL146192, U01-HL146194]
- National Institute on Minority Health and Health Disparities
- NIH, Office of AIDS Research
- NIH [UL1-TR003098, UL1-TR001881, P30-AI-050409, UL1-TR000004, P30-AI-073961, P30-AI-050410, P30-AI-027767, P30-MH-116867]
- National Heart, Lung, and Blood Institute
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- National Institute on Aging
- National Institute of Dental and Craniofacial Research
- National Institute of Allergy and Infectious Diseases
- National Institute of Neurological Disorders and Stroke
- National Institute of Mental Health
- National Institute on Drug Abuse
- National Institute of Nursing Research
- National Cancer Institute
- National Institute on Alcohol Abuse and Alcoholism
- National Institute on Deafness and Other Communication Disorders
- National Institute of Diabetes and Digestive and Kidney Diseases
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Menopause may lead to increased innate immune activation in women with HIV, but does not affect gut barrier or inflammation. Further research is needed to investigate the clinical significance of immune activation during the menopausal transition.
Background. Persistent immune activation due to gut barrier dysfunction is a suspected cause of morbidity in HIV, but the impact of menopause on this pathway is unknown. Methods. In 350 women with HIV from the Women's Interagency HIV Study, plasma biomarkers of gut barrier dysfunction (intestinal fatty acid binding protein; IFAB), innate immune activation (soluble CD14 and CD163; sCD14, 5CD163), and systemic inflammation (interleukin-6 and tumor necrosis factor receptor 1; IL-6, TNFR1) were measured at 674 person-visits spanning <= 2 years. Results. Menopause (post- vs premenopausal status) was associated with higher plasma sCD14 and sCD163 in linear mixed-effects regression adjusting for age and other covariates (beta = 161.89 ng/mL; 95% confidence interval [CI], 18.37-305.41 and 65.48 ng/mL, 95% CI, 6.64-124.33, respectively); but not with plasma IFAB, IL-6, or TNFR1. In piece-wise linear mixed-effects regression of biomarkers on years before/after the final menstrual period, sCD14 increased during the menopausal transition by 250.71 ng/mL per year (95% CI, 16.63-484.79; P = .04), but not in premenopausal or postmenopausal periods. Conclusions. In women with HIV, menopause may increase innate immune activation, but data did not support an influence on the gut barrier or inflammation. Clinical implications of immune activation during menopausal transition warrant further investigation.
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