ArticleScientific reports2018
High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 49 citations in OpenAlex.
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- Enhanced Rapid Screening for Multidrug-resistant tuberculosis through combined cardiometabolic and inflammatory indices: a cross-sectional study.Scientific reports · 2024Article
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- Associations between type 1 diabetes and pulmonary tuberculosis: a bidirectional mendelian randomization study.Diabetology & metabolic syndrome · 2024Article
- Association between biomarkers of inflammation and dyslipidemia in drug resistant tuberculosis in Uganda.Lipids in health and disease · 2024Article
- Single-cell analysis reveals a weak macrophage subpopulation response to Mycobacterium tuberculosis infection.Cell reports · 2023Article
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- Correlation of apolipoprotein A-I with T cell subsets and interferon-ү in coronary artery disease.Immunity, inflammation and disease · 2023Article
- Low-Density Lipoprotein Contributes to Endometrial Carcinoma Cell Proliferation, Migration, and Invasion by Activating the JAK-STAT Signaling Pathway.Analytical cellular pathology (Amsterdam) · 2023Article
- Association between metabolic syndrome and osteoporosis among adults aged 50 years and older: using the National Health Information Database in South Korea.Archives of osteoporosis · 2022Article
- Monitoring IgG against Mycobacterium tuberculosis proteins in an Asian elephant cured of tuberculosis that developed from long-term latency.Scientific reports · 2022Article
- Article
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- The role of high-density lipoprotein in the regulation of the immune response: implications for atherosclerosis and autoimmunity.Immunology · 2021Review
- Development of Metabolic Syndrome Decreases Bone Mineral Density T-Score of Calcaneus in Foot in a Large Taiwanese Population Follow-Up Study.Journal of personalized medicine · 2021Article
- Lipoarabinomannan as a Point-of-Care Assay for Diagnosis of Tuberculosis: How Far Are We to Use It?Frontiers in microbiology · 2021Review
- Protein and Microbial Biomarkers in Sputum Discern Acute and Latent Tuberculosis in Investigation of Pastoral Ethiopian Cohort.Frontiers in cellular and infection microbiology · 2021Article
- Cardiovascular disease risk factors and markers of oxidative stress and DNA damage in leprosy patients in Southern Nigeria.PLoS neglected tropical diseases · 2020Article
- Comprehensive plasma proteomic profiling reveals biomarkers for active tuberculosis.JCI insight · 2020Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune responses to parasitic pathogens are affected by the host physiological condition. High-density lipoprotein (HDL) and low-density lipoprotein (LDL) are transporters of lipids between the liver and peripheral tissues, and modulate pro-inflammatory immune responses. Pathogenic mycobacteria are parasitic intracellular bacteria that can survive within macrophages for a long period. Macrophage function is thus key for host defense against mycobacteria. These basic facts suggest possible effects of HDL and LDL on mycobacterial diseases, which have not been elucidated so far. In this study, we found that HDL and not LDL enhanced mycobacterial infections in human macrophages. Nevertheless, we observed that HDL remarkably suppressed production of tumor necrosis factor alpha (TNF-α) upon mycobacterial infections. TNF-α is a critical host-protective cytokine against mycobacterial diseases. We proved that toll-like receptor (TLR)-2 is responsible for TNF-α production by human macrophages infected with mycobacteria. Subsequent analysis showed that HDL downregulates TLR2 expression and suppresses its intracellular signaling pathways. This report demonstrates for the first time the substantial action of HDL in mycobacterial infections to human macrophages.
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