Trial reportScientific reports2021
PGE2 displays immunosuppressive effects during human active tuberculosis.
Trial report in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 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
18 citing papers in PubMed, 31 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
- Mycobacterium tuberculosis-induced PCBP1 degradation drives macrophage ferroptosis to promote infection: a lung-macrophage-targeted RNAa nanotherapy.Journal of nanobiotechnology · 2026Article
- Glutaminase 1-mediated glutaminolysis regulates tuberculosis progression by modulating Th1 and Th17 immune responses.Central-European journal of immunology · 2026Article
- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Host-directed therapy for tuberculosis.European journal of medical research · 2025Review
- Dual GSK-3β/HDAC Inhibitors Enhance the Efficacy of Macrophages to ControlBiomolecules · 2025Article
- Exploring Oxylipins in Host-Microbe Interactions and Their Impact on Infection and Immunity.Current issues in molecular biology · 2025Review
- Article
- Where lung cancer and tuberculosis intersect: recent advances.Frontiers in immunology · 2025Review
- Lessons from cross-pathogen studies: understanding the metabolic rewiring of macrophages upon infection.Frontiers in cellular and infection microbiology · 2025Review
- Review
- Cancer and Autoimmune Diseases as Two Sides of Chronic Inflammation and the Method of Therapy.Current cancer drug targets · 2024Review
- Expression of Prostaglandin Genes and β-Catenin in Whole Blood as Potential Markers of Muscle Degeneration.International journal of molecular sciences · 2023Article
- Dynamics of inflammatory cytokine expression in bovine endometrial cells exposed to cow blood plasma small extracellular vesicles (sEV) may reflect high fertility.Scientific reports · 2023Article
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Effect of Dysglycemia on Urinary Lipid Mediator Profiles in Persons With Pulmonary Tuberculosis.Frontiers in immunology · 2022Observational
- Article
- Shedding Light on Autophagy During Human Tuberculosis. A Long Way to Go.Frontiers in cellular and infection microbiology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandin E2 (PGE2), an active lipid compound derived from arachidonic acid, regulates different stages of the immune response of the host during several pathologies such as chronic infections or cancer. In fact, manipulation of PGE2 levels was proposed as an approach for countering the Type I IFN signature of tuberculosis (TB). However, very limited information regarding the PGE2 pathway in patients with active TB is currently available. In the present work, we demonstrated that PGE2 exerts a potent immunosuppressive action during the immune response of the human host against Mycobacterium tuberculosis (Mtb) infection. Actually, we showed that PGE2 significantly reduced the surface expression of several immunological receptors, the lymphoproliferation and the production of proinflammatory cytokines. In addition, PGE2 promoted autophagy in monocytes and neutrophils cultured with Mtb antigens. These results suggest that PGE2 might be attenuating the excessive inflammatory immune response caused by Mtb, emerging as an attractive therapeutic target. Taken together, our findings contribute to the knowledge of the role of PGE2 in the human host resistance to Mtb and highlight the potential of this lipid mediator as a tool to improve anti-TB treatment.
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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.