ArticleInfection and immunity2008
Hypercholesterolemia impairs immunity to tuberculosis.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
88 citing papers in PubMed, 153 citations in OpenAlex.
- All-trans retinoic acid-triggered antimicrobial activity against Mycobacterium tuberculosis is dependent on NPC2.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- The Proteome of Plasma Extracellular Vesicles in Latent and Active Tuberculosis Reveals Phase-Specific Composition and Immunometabolic Insights.FASEB bioAdvances · 2026Article
- QuantiFERON-TB Gold Plus Conversion Among Healthcare Workers: A Retrospective Cohort Study on Occupational and Metabolic Factors.Healthcare (Basel, Switzerland) · 2026Article
- Machine learning prediction of tuberculosis mortality: a comparative analysis of random survival forest and cox regression models.BMC infectious diseases · 2026Article
- Low-density lipoprotein cholesterol drives multinucleated giant cell formation in response to mycobacterium bovis Bacille Calmette-Guérin.Scientific reports · 2026Article
- Type I IFN drives neutrophil swarming, impeding lung T cell-macrophage interactions and TB control.The Journal of experimental medicine · 2025Article
- Diet-induced dyslipidemia enhances IFN-γ production in mycolic acid-specific T cells and affects mycobacterial control.Mucosal immunology · 2025Article
- The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities.Infectious disease reports · 2025Review
- APOE protects against severe infection with Mycobacterium tuberculosis by restraining production of neutrophil extracellular traps.PLoS pathogens · 2025Article
- Dyslipidemia and female reproductive failures: perspectives on lipid metabolism and endometrial immune dysregulation.Seminars in immunopathology · 2025Review
- Decreased mRNA expression of NR1H3 and ABCA1 in pulmonary tuberculosis patients from population of Punjab, India.Molecular biology reports · 2024Article
- G9a and Sirtuin6 epigenetically modulate host cholesterol accumulation to facilitate mycobacterial survival.PLoS pathogens · 2023Article
- A multiple comorbidities mouse lung infection model inBiomedical reports · 2023Article
- Repurposing of statins for Buruli Ulcer treatment: antimicrobial activity againstFrontiers in microbiology · 2023Article
- Sterols and immune mechanisms in asthma.The Journal of allergy and clinical immunology · 2023Review
- Roles of cysteine in the structure and metabolic function ofRSC advances · 2022Article
- AllCurrent research in immunology · 2022Review
- Multiple aspects of lymphatic dysfunction in anFrontiers in physiology · 2022Article
- Identification of protein biomarkers in host cerebrospinal fluid for differential diagnosis of tuberculous meningitis and other meningitis.Frontiers in neurology · 2022Article
- Respiratory Tract Infections in Diabetes - Lessons From Tuberculosis and Influenza to Guide Understanding of COVID-19 Severity.Frontiers in endocrinology · 2022Review
28 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We demonstrate that apolipoprotein E -deficient (ApoE(-/-)) mice are highly susceptible to tuberculosis and that their susceptibility depends on the severity of hypercholesterolemia. Wild-type (WT) mice and ApoE(-/-) mice fed a low-cholesterol (LC) or high-cholesterol (HC) diet were infected with approximately 50 CFU Mycobacterium tuberculosis Erdman by aerosol. ApoE(-/-) LC mice were modestly more susceptible to tuberculosis than WT LC mice. In contrast, ApoE(-/-) HC mice were extremely susceptible, as evidenced by 100% mortality after 4 weeks with tuberculosis. The lung pathology of ApoE(-/-) HC mice was remarkable for giant abscess-like lesions, massive infiltration by granulocytes, elevated inflammatory cytokine production, and a mean bacterial load approximately 2 log units higher than that of WT HC mice. Compared to WT HC mice, the gamma interferon response of splenocytes restimulated ex vivo with M. tuberculosis culture filtrate protein was delayed in ApoE(-/-) HC mice, and they failed to control M. tuberculosis growth in the lung. OT-II cells adoptively transferred into uninfected ApoE(-/-) HC mice had a weak proliferative response to their antigen, indicating impaired priming of the adaptive immune response. Our studies show that ApoE(-/-) deficiency is associated with delayed expression of adaptive immunity to tuberculosis caused by defective priming of the adaptive immune response and that elevated serum cholesterol is responsible for this effect.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.