ArticleTuberculosis (Edinburgh, Scotland)2018
Deletion of PPARγ in lung macrophages provides an immunoprotective response against M. tuberculosis infection in mice.
Article in Tuberculosis (Edinburgh, Scotland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Mycobacterium tuberculosis IDH-PPARγ interaction suppresses GPX4 to drive macrophage ferroptosis and sustain persistent infection.Nature communications · 2026Article
- The signaling pathway of PPAR-γ and its protective role in various diseases.Caspian journal of internal medicine · 2026Review
- NR4A nuclear receptor expression in human macrophages mediates apoptosis and controls Mycobacterium tuberculosis growth.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The Regulatory Network of Transcription Factors in Macrophage Polarization.ImmunoTargets and therapy · 2025Review
- Macrophages exploit the mannose receptor and JAK-STAT1-MHC-II pathway to drive antigen presentation and the antimycobacterial immune response after BCG vaccination.Acta biochimica et biophysica Sinica · 2024Article
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- Turning foes into permissive hosts: manipulation of macrophage polarization by intracellular bacteria.Current opinion in immunology · 2023Review
- Article
- IL-10 Modulation Increases Pyrazinamide's Antimycobacterial Efficacy against Mycobacterium tuberculosis Infection in Mice.ImmunoHorizons · 2023Article
- A new tractable method for generating Human Alveolar Macrophage Like cells in vitro to study lung inflammatory processes and diseases.bioRxiv : the preprint server for biology · 2023Article
- Microglia and Cholesterol Handling: Implications for Alzheimer's Disease.Biomedicines · 2022Review
- Surveying the Epigenetic Landscape of Tuberculosis in Alveolar Macrophages.Infection and immunity · 2022Review
- Tuberculosis alters immune-metabolic pathways resulting in perturbed IL-1 responses.Frontiers in immunology · 2022Article
- The Impact of Aging on the Lung Alveolar Environment, Predetermining Susceptibility to Respiratory Infections.Frontiers in aging · 2022Review
- Essential Roles of PPARs in Lipid Metabolism during Mycobacterial Infection.International journal of molecular sciences · 2021Review
- Role of specialized pro-resolving lipid mediators in pulmonary inflammation diseases: mechanisms and development.Respiratory research · 2021Review
- Macrophage-derived cytokines in pneumonia: Linking cellular immunology and genetics.Cytokine & growth factor reviews · 2021Review
- Review
- PPAR Gamma: From Definition to Molecular Targets and Therapy of Lung Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear transcription factor belonging to the superfamily of ligand-activated nuclear receptors. It is activated by diverse endogenous lipid metabolites as well as by exogenous ligands such as the thiazolidinediones. It regulates cellular metabolism, proliferation, differentiation, and inflammation, the latter in part through trans-repression of pro-inflammatory cytokines. PPARγ is highly expressed in alternatively activated alveolar macrophages (AMs), a primary host cell for airborne Mycobacterium tuberculosis (M.tb). Our previous in vitro study identified the importance of PPARγ activation through the mannose receptor (CD206) on human macrophages in enabling M. tb growth. The aim of the current study was to investigate the role of PPARγ in vivo during M. tb infection using a macrophage-specific PPARγ knock out mouse model with special emphasis on the lung environment. Our data show that the absence of PPARγ in lung macrophages reduces the growth of virulent M. tb, enhances pro-inflammatory cytokines and reduces granulomatous infiltration. These findings demonstrate that PPARγ activation, which down-regulates macrophage pro-inflammatory responses, impacts the lung's response to M. tb infection, thereby supporting PPARγ's role in tuberculosis (TB) pathogenesis.
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.