ReviewJournal of innate immunity2017
Participation of Necroptosis in the Host Response to Acute Bacterial Pneumonia.
Review in Journal of innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 42 citations in OpenAlex.
- Decoding Host-Pathogen Dynamics inAntibiotics (Basel, Switzerland) · 2026Review
- Regulatory complexity and therapeutic targeting of the necroptosis network.Frontiers in immunology · 2026Review
- Peptide GTSFTTTAER FromFood science & nutrition · 2025Article
- Insights into the roles of macrophages in Klebsiella pneumoniae infections: a comprehensive review.Cellular & molecular biology letters · 2025Review
- Erythronecroptosis: an overview of necroptosis or programmed necrosis in red blood cells.Molecular and cellular biochemistry · 2024Review
- A narrative review on lung injury: mechanisms, biomarkers, and monitoring.Critical care (London, England) · 2024Review
- Targeting necroptosis: a promising avenue for respiratory disease treatment.Cell communication and signaling : CCS · 2024Review
- Interactions and Implications ofInfection and drug resistance · 2024Review
- Autophagy, cell death, and cytokines inEmerging microbes & infections · 2023Review
- TREM-1 triggers necroptosis of macrophages through mTOR-dependent mitochondrial fission during acute lung injury.Journal of translational medicine · 2023Article
- Regulated necrosis, a proinflammatory cell death, potentially counteracts pathogenic infections.Cell death & disease · 2022Review
- The role of necroptosis in common respiratory diseases in children.Frontiers in pediatrics · 2022Review
- Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease.Annals of medicine · 2021Review
- Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- RIPK3 Activates MLKL-mediated Necroptosis and Inflammasome Signaling duringAmerican journal of respiratory cell and molecular biology · 2021Article
- Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation.Cell reports · 2020Article
- Using More Than 1 (Path)Way to Kill a Host Cell: Lessons FromMicrobiology insights · 2020Article
- Competitive Cell Death Interactions in Pulmonary Infection: Host Modulation Versus Pathogen Manipulation.Frontiers in immunology · 2020Review
- RIP1, RIP3, and MLKL Contribute to Cell Death Caused by Clostridium perfringens Enterotoxin.mBio · 2019Article
- Flipping the dogma - phosphatidylserine in non-apoptotic cell death.Cell communication and signaling : CCS · 2019Review
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 at 2 institutions in 1 country.
Funding
Abstract
Common pulmonary pathogens, such as Streptococcus pneumoniae and Staphylococcus aureus, as well as the host-adapted pathogens responsible for health care-associated pneumonias, such as the carbapenem-resistant Klebsiella pneumoniae and Serratia marcecsens, are able to activate cell death through the RIPK1/RIPK3/MLKL cascade that causes necroptosis. Necroptosis can influence the pathogenesis of pneumonia through several mechanisms. Activation of this pathway can result in the loss of specific types of immune cells, especially macrophages, and, in so doing, contribute to host pathology through the loss of their critical immunoregulatory functions. However, in other settings of infection, necroptosis promotes pathogen removal and the eradication of infected cells to control excessive proinflammatory signaling. Bacterial production of pore-forming toxins provides a common mechanism to activate necroptosis by diverse bacterial species, with variable consequences depending upon the specific pathogen. Included in this brief review are data demonstrating the ability of the carbapenem-resistant ST258 K. pneumoniae to activate necroptosis in the setting of pneumonia, which is counterbalanced by their suppression of CYLD expression. Exactly how necroptosis and other mechanisms of cell death are coregulated in the response to specific pulmonary pathogens remains a topic of active investigation, and it may provide potential therapeutic targets in the future.
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.