ArticlePLoS pathogens2024
Suppressing neutrophil itaconate production attenuates Mycoplasma pneumoniae pneumonia.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Neutrophil-to-lymphocyte ratio for predicting disease severity and outcomes in children with Mycoplasma pneumoniae pneumonia: a systematic review and meta-analysis.BMC pulmonary medicine · 2026Pooled it
- Clinical study on improving lung function in children after Mycoplasma pneumoniae pneumonia (MMP) via traditional Chinese medicine meridian massage.BMC pediatrics · 2026Trial
- Neutrophil-to-lymphocyte ratio mediates pulmonary consolidation through oxidative stress in children withAnnals of medicine · 2026Article
- Itaconate metabolism in regulated cell death.Molecular and cellular biochemistry · 2026Review
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Remote electroacupuncture conditioning protects the heart via fine-tuning the dual role of the SDF-1α/CXCR4 axis in myocardial ischemia-reperfusion injury.Chinese medicine · 2026Article
- Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Correlation analysis of FABP3, MCP-4, and CXCL9 levels and myocardial damage in patients with severe pneumonia.Journal of medical biochemistry · 2026Article
- Dysregulation of Neutrophil-Endothelial Communication in Sepsis: Mechanisms and Therapeutic Perspectives.Cells · 2026Review
- Host immune dysfunction and Mycoplasma pneumoniae immune evasion: dual drivers of pathogenesis in Mycoplasma pneumoniae pneumonia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Nasal delivery ofMicrobiology spectrum · 2026Article
- Development of a Prediction Model for Severe PediatricInfection and drug resistance · 2026Article
- Nuclear IL-33 amplifies NF-κB signaling to drive neutrophil recruitment and activation in the endocervical epithelium duringFrontiers in immunology · 2026Article
- Analysis of Plasma Biomarkers and Potential Pathogenesis in Children withInfection and drug resistance · 2026Article
- IRG1-itaconate axis in immunometabolism: mechanistic roles and therapeutic potential in inflammatory diseases.Frontiers in immunology · 2026Review
- Advances in infection-immunity mechanisms and molecular regulatory networks in severe pneumonia-associated lung injury.Frontiers in immunology · 2026Review
- MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy.Frontiers in pediatrics · 2026Article
- Comparative progress on the mechanisms of airway mucosal injury induced by different pathogens: SARS-CoV-2, influenza A virus, and Mycoplasma pneumoniae.Frontiers in cellular and infection microbiology · 2026Review
- Intermittent hypoxia drives lung microbiome-metabolome remodeling to create a pro-inflammatory landscape in murine OSAHS.Frontiers in microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycoplasma pneumoniae is a common cause of community-acquired pneumonia in which neutrophils play a critical role. Immune-responsive gene 1 (IRG1), responsible for itaconate production, has emerged as an important regulator of inflammation and infection, but its role during M. pneumoniae infection remains unknown. Here, we reveal that itaconate is an endogenous pro-inflammatory metabolite during M. pneumoniae infection. Irg1 knockout (KO) mice had lower levels of bacterial burden, lactate dehydrogenase (LDH), and pro-inflammatory cytokines compared with wild-type (WT) controls after M. pneumoniae infection. Neutrophils were the major cells producing itaconate during M. pneumoniae infection in mice. Neutrophil counts were positively correlated with itaconate concentrations in bronchoalveolar lavage fluid (BALF) of patients with severe M. pneumoniae pneumonia. Adoptive transfer of Irg1 KO neutrophils, or administration of β-glucan (an inhibitor of Irg1 expression), significantly attenuated M. pneumoniae pneumonia in mice. Mechanistically, itaconate impaired neutrophil bacterial killing and suppressed neutrophil apoptosis via inhibiting mitochondrial ROS. Moreover, M. pneumoniae induced Irg1 expression by activating NF-κB and STAT1 pathways involving TLR2. Our data thus identify Irg1/itaconate pathway as a potential therapeutic target for the treatment of M. pneumoniae pneumonia.
Indexed as
Identifiers
What Socratic 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 Socratic graph.