ReviewAdvances in experimental medicine and biology2013
Dying to live: how the death modality of the infected macrophage affects immunity to tuberculosis.
Review in Advances in experimental medicine and biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
71 citing papers in PubMed, 117 citations in OpenAlex.
- The Cyclooxygenase 2 Inhibitor Etoricoxib as Adjunctive Therapy in Tuberculosis Impairs Macrophage Control of Mycobacterial Growth.The Journal of infectious diseases · 2024Trial
- Plasma LOX-Products and Monocyte Signaling Is Reduced by Adjunctive Cyclooxygenase-2 Inhibitor in a Phase I Clinical Trial of Tuberculosis Patients.Frontiers in cellular and infection microbiology · 2021Trial
- The antimycobacterial and healing effect of sorafenib through pro-apoptotic and immunomodulatory activities.Microbiology spectrum · 2026Article
- Mycobacterium tuberculosis triggers reduced inflammatory cytokine responses and virulence in mice lacking Tax1bp1.PLoS pathogens · 2025Article
- Delineating the Significance of Several Inflammatory Markers in a Lung Tuberculosis Cohort During the Active and Post-Tuberculosis Stages of the Disease: An Observational Study in Cape Town, South Africa (2019 to 2024).Infectious disease reports · 2025Article
- S-nitrosylation-triggered secretion of mycobacterial PknG leads to phosphorylation of SODD to prevent apoptosis of infected macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Abnormalities of lipid metabolism in the progression and treatment of depression.Frontiers in psychiatry · 2025Review
- Model systems to studyFrontiers in cellular and infection microbiology · 2025Review
- Tax1bp1 enhances bacterial virulence and promotes inflammatory responses duringbioRxiv : the preprint server for biology · 2024Article
- A cytoprotective role for optineurin during mycobacterial infection of macrophages.Biochemistry and biophysics reports · 2024Article
- Metabolic changes enhance necroptosis of type 2 diabetes mellitus mice infected with Mycobacterium tuberculosis.PLoS pathogens · 2024Article
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- Identification and Validation of Genes Related to Macrophage Polarization and Cell Death Modes UnderJournal of inflammation research · 2024Article
- High Bacillary Burden and the ESX-1 Type VII Secretion System Promote MHC Class I Presentation by Mycobacterium tuberculosis-Infected Macrophages to CD8 T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Adjunctive Integrated Stress Response Inhibition Accelerates Tuberculosis Clearance in Mice.mBio · 2023Article
- Atg8ylation as a host-protective mechanism againstFrontiers in tuberculosis · 2023Article
- Lipid droplets as multifunctional organelles related to the mechanism of evasion during mycobacterial infection.Frontiers in cellular and infection microbiology · 2023Review
- Article
- Virulence-Associated Secretion inFrontiers in immunology · 2022Review
- Macrophage: A Cell With Many Faces and Functions in Tuberculosis.Frontiers in immunology · 2022Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Virulent Mycobacterium tuberculosis (Mtb) inhibits apoptosis and triggers necrosis of host macrophages to evade innate delay in the initiation of adaptive immunity. Necrosis is a mechanism used by bacteria to exit macrophage, evade the host defenses, and disseminate while apoptosis is associated with diminished pathogen viability. We have recently demonstrated that eicosanoids regulate cell death program of either human or murine macrophages infected with Mtb. We have defined prostaglandin E2 (PGE2) as a pro-apoptotic host lipid mediator which protects against necrosis. In contrast, lipoxin A4 (LXA4) is a pro-necrotic lipid mediator which suppresses PGE2 synthesis, resulting in mitochondrial damage and inhibition of plasma membrane repair mechanisms; this ultimately leads to the induction of necrosis. Thus, the balance between PGE2 and LXA4 determines whether Mtb-infected macrophages undergo apoptosis or necrosis and this balance determines the outcome of infection.
Indexed as
Identifiers
What OpenQuestion holds
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.