ArticleThe Journal of clinical investigation2018
Disruption of staphylococcal aggregation protects against lethal lung injury.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 50 citations in OpenAlex.
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- Multivalent nanobodies for potent and broad neutralization of Staphylococcus aureus toxins.Nature communications · 2026Article
- Extracellular Vesicles Coordinate Bacterial Cloaking in Lung Epithelial Cells to Alleviate Acute Inflammatory Injury.Journal of extracellular vesicles · 2026Article
- A Prediction Model for Persistent Inflammation-Immunosuppression-Catabolism Syndrome in Patients with Sepsis: An Ambispective Cohort Study.Infection and drug resistance · 2026Article
- Macrophage-specific therapy blocks the lung's mechanosensitive immune response to alveolar distension.JCI insight · 2025Article
- Alpha-toxin-elicited CXmBio · 2025Article
- Acute Respiratory Distress Syndrome: Pathophysiological Insights, Subphenotypes, and Clinical Implications-A Comprehensive Review.Journal of clinical medicine · 2025Review
- Mechanistic insights into the multitarget synergistic efficacy of farrerol and β-lactam antibiotics in combating methicillin-resistantAntimicrobial agents and chemotherapy · 2025Article
- CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Microenvironmental acidification by pneumococcal sugar consumption fosters barrier disruption and immune suppression in the human alveolus.The European respiratory journal · 2024Article
- Stem cells, cell therapies, and bioengineering in lung biology and diseases 2023.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- The role of human extracellular matrix proteins in defining Staphylococcus aureus biofilm infections.FEMS microbiology reviews · 2024Review
- The pathogenesis of influenza in intact alveoli: virion endocytosis and its effects on the lung's air-blood barrier.Frontiers in immunology · 2024Review
- Rescue of alveolar wall liquid secretion blocks fatal lung injury due to influenza-staphylococcal coinfection.The Journal of clinical investigation · 2023Article
- Advancements in the Management of Severe Community-Acquired Pneumonia: A Comprehensive Narrative Review.Cureus · 2023Review
- Mitochondria of lung venular capillaries mediate lung-liver cross talk in pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Nuclease activity and protein A release ofFrontiers in immunology · 2023Article
- WYBQ-4: a New Bactericidal Agent against Methicillin-Resistant Staphylococcus aureus.Microbiology spectrum · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Infection by Staphylococcus aureus strain USA300 causes tissue injury, multiorgan failure, and high mortality. However, the mechanisms by which the bacteria adhere to, then stabilize on, mucosal surfaces before causing injury remain unclear. We addressed these issues through the first real-time determinations of USA300-alveolar interactions in live lungs. We found that within minutes, inhaled USA300 established stable, self-associated microaggregates in niches at curved, but not at flat, regions of the alveolar wall. The microaggregates released α-hemolysin toxin, causing localized alveolar injury, as indicated by epithelial dye loss, mitochondrial depolarization, and cytosolic Ca2+ increase. Spread of cytosolic Ca2+ through intercellular gap junctions to adjoining, uninfected alveoli caused pulmonary edema. Systemic pretreatment with vancomycin, a USA300-cidal antibiotic, failed to protect mice infected with inhaled WT USA300. However, vancomycin pretreatment markedly abrogated mortality in mice infected with mutant USA300 that lacked the aggregation-promoting factor PhnD. We interpret USA300-induced mortality as having resulted from rapid bacterial aggregation in alveolar niches. These findings indicate, for the first time to our knowledge, that alveolar microanatomy is critical in promoting the aggregation and, hence, in causing USA300-induced alveolar injury. We propose that in addition to antibiotics, strategies for bacterial disaggregation may constitute novel therapy against USA300-induced lung injury.
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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.