ArticlePLoS pathogens2023
Pseudomonas aeruginosa pulmonary infection results in S100A8/A9-dependent cardiac dysfunction.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Plasma proteomics identifies S100A8/A9 as a novel biomarker and therapeutic target for fulminant myocarditis.Journal of advanced research · 2026Article
- Article
- Article
- Think Locally, Act Globally: Resolving the Peripheral Immune Milieu in Bacterial Pneumonia.American journal of respiratory and critical care medicine · 2025Article
- S100A8/9-NLRP3-mediated chronic unresolved inflammation drives cardiac pathologies following invasive pneumococcal disease.Experimental & molecular medicine · 2025Article
- Multi-omics driven biomarker discovery and pathological insights into Pseudomonas aeruginosa pneumonia.BMC infectious diseases · 2025Article
- Decoding mechanisms and protein markers in lung-brain axis.Respiratory research · 2025Review
- Impact of pulmonary infection and antibiotic use on recurrent myocardial infarction in patients with myocardial infarction.Scientific reports · 2025Article
- Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction.Current issues in molecular biology · 2024Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Pseudomonas aeruginosa (P.a.) infection accounts for nearly 20% of all cases of hospital acquired pneumonia with mortality rates >30%. P.a. infection induces a robust inflammatory response, which ideally enhances bacterial clearance. Unfortunately, excessive inflammation can also have negative effects, and often leads to cardiac dysfunction with associated morbidity and mortality. However, it remains unclear how P.a. lung infection causes cardiac dysfunction. Using a murine pneumonia model, we found that P.a. infection of the lungs led to severe cardiac left ventricular dysfunction and electrical abnormalities. More specifically, we found that neutrophil recruitment and release of S100A8/A9 in the lungs activates the TLR4/RAGE signaling pathways, which in turn enhance systemic inflammation and subsequent cardiac dysfunction. Paradoxically, global deletion of S100A8/A9 did not improve but aggravated cardiac dysfunction and mortality likely due to uncontrolled bacterial burden in the lungs and heart. Our results indicate that P.a. infection induced release of S100A8/9 is double-edged, providing increased risk for cardiac dysfunction yet limiting P.a. growth.
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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.