ReviewRespiratory research2020
Airway immunometabolites fuel Pseudomonas aeruginosa infection.
Review in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed.
- Convergent evolution of immune evasion in ESKAPE pathogens: A cross-pathogen architecture of conserved host-defense checkpoints.European journal of microbiology & immunology · 2026Review
- Isoflavones with Multifaceted Activities Synergistically SensitizeAntibiotics (Basel, Switzerland) · 2026Article
- Calcium regulation ofApplied and environmental microbiology · 2026Article
- Volatile organic compound profiling for tracking clinical Pseudomonas aeruginosa isolates.Scientific reports · 2026Article
- Article
- Mutations in filamentous bacteriophages spark eco-evolutionary feedbacks in Pseudomonas aeruginosa.The ISME journal · 2026Article
- Succinate-driven virulence enhancement in hypervirulentMicrobiology spectrum · 2026Article
- The TREM2 paradox in fibrosis: a unified mechanism for opposite outcomes across organs.Frontiers in immunology · 2026Review
- Sequestration of the phagocyte metabolite itaconate by Pseudomonas aeruginosa RpoN promotes successful pulmonary infection.Nature communications · 2025Article
- Carbon source-driven downregulation of the sRNA AmiL enhancesVirulence · 2025Article
- Itaconate utilisation by the human pathogen Pseudomonas aeruginosa requires uptake via the IctPQM TRAP transporter.The Biochemical journal · 2025Article
- Multi-omics driven biomarker discovery and pathological insights into Pseudomonas aeruginosa pneumonia.BMC infectious diseases · 2025Article
- Genetically Diverse Mycobacterium tuberculosis Isolates Manipulate Inflammasome and Interleukin 1β Secretion Independently of Macrophage Metabolic Rewiring.The Journal of infectious diseases · 2025Article
- Molecular mechanisms and therapeutic targets of acute exacerbations of chronic obstructive pulmonary disease with Pseudomonas aeruginosa infection.Respiratory research · 2025Article
- Article
- Hypoxia-inducible factor-driven glycolytic adaptations in host-microbe interactions.Pflugers Archiv : European journal of physiology · 2024Review
- Insights into the Synergistic Antibacterial Activity of Silver Nitrate with Potassium Tellurite againstMicrobiology spectrum · 2023Article
- A succinate/SUCNR1-brush cell defense program in the tracheal epithelium.Science advances · 2023Article
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
- Training vs. Tolerance: The Yin/Yang of the Innate Immune System.Biomedicines · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Pulmonary infections are associated with a brisk inflammatory reaction to bacterial surface components. Lipopolysaccharides (LPS) trigger macrophage activation and release of mitochondrial metabolites that control the intensity of the immune response. Whereas succinate induces oxidative stress (ROS), HIF1α stabilization, glycolysis and IL-1β release, itaconate suppresses inflammation by inhibiting succinate oxidation, glycolytic flux and promoting anti-oxidant Nrf2-HO-1 functions. P. aeruginosa is a major pathogen associated with acute and chronic lung infection. Although both secreted toxins, LPS and proteases are key factors to establish acute P. aeruginosa pneumonia, lack of these components in chronic P. aeruginosa isolates suggest these organisms exploit other mechanisms to adapt and persist in the lung. Upon inhalation, P. aeruginosa strains trigger airway macrophage reprograming and bacterial variants obtained from acutely and chronically infected subjects exhibit metabolic adaptation consistent with succinate and itaconate assimilation; namely, high expression of extracellular polysaccharides (EPS), reduced lptD-LPS function, increased glyoxylate shunt (GS) activity and substantial biofilm production. In this review we discuss recent findings illustrating how P. aeruginosa induces and adapts to macrophage metabolites in the human lung, and that catabolism of succinate and itaconate contribute to their formidable abilities to tolerate oxidative stress, phagocytosis and immune clearance.
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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.