ArticleInternational journal of molecular sciences2023
Can Neutrophils Prevent Nosocomial Pneumonia after Serious Injury?
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Structural and molecular principles of DAMP biology.Nature structural & molecular biology · 2026Review
- Transcriptomics reveals the underlying mechanism of Prostaglandin E1 in improving severe pneumonia.BMC pulmonary medicine · 2025Article
- C/EBPε and its acetylation in PMN enhance the tolerance to trauma.Clinical and experimental immunology · 2025Article
- Construction of a prediction model for pneumonia in children undergoing neurosurgery based on regular clinical laboratory tests and baseline information.Frontiers in pediatrics · 2025Article
- The immune suppressive properties of damage associated molecular patterns in the setting of sterile traumatic injury.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Nosocomial pneumonia is a leading cause of critical illness and mortality among seriously injured trauma patients. However, the link between injury and the development of nosocomial pneumonia is still not well recognized. Our work strongly suggests that mitochondrial damage-associated molecular patterns (mtDAMPs), especially mitochondrial formyl peptides (mtFPs) released by tissue injury, play a significant role in developing nosocomial pneumonia after a serious injury. Polymorphonuclear leukocytes (neutrophils, PMN) migrate toward the injury site by detecting mtFPs through formyl peptide receptor 1 (FPR1) to fight/contain bacterial infection and clean up debris. Activation of FPR1 by mtFPs enables PMN to reach the injury site; however, at the same time it leads to homo- and heterologous desensitization/internalization of chemokine receptors. Thus, PMN are not responsive to secondary infections, including those from bacteria-infected lungs. This may enable a progression of bacterial growth in the lungs and nosocomial pneumonia. We propose that the intratracheal application of exogenously isolated PMN may prevent pneumonia coupled with a serious injury.
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Registered trials
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