ArticleThe journal of trauma and acute care surgery2014
Mitochondrial damage-associated molecular patterns released by abdominal trauma suppress pulmonary immune responses.
Article in The journal of trauma and acute care surgery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Formyl peptide receptor 1 agonism selectively suppresses mitochondria-driven neutrophil extracellular trap formation while preserving antibacterial immunity.Molecular medicine (Cambridge, Mass.) · 2026Article
- Cannabidiol mitigates secondary genital injury after thoracic trauma by regulating systemic inflammation and hormone receptor signaling.Scientific reports · 2026Article
- Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole.Antioxidants (Basel, Switzerland) · 2024Review
- Can Neutrophils Prevent Nosocomial Pneumonia after Serious Injury?International journal of molecular sciences · 2023Article
- The immune suppressive properties of damage associated molecular patterns in the setting of sterile traumatic injury.Frontiers in immunology · 2023Review
- Understanding the role of neutrophils in acute respiratory distress syndrome.Biomedical journal · 2021Review
- Circulating mitochondrialProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Formyl Peptide Receptor-1 Blockade Prevents Receptor Regulation by Mitochondrial Danger-Associated Molecular Patterns and Preserves Neutrophil Function After Trauma.Critical care medicine · 2020Article
- Circulating mitochondria in deceased organ donors are associated with immune activation and early allograft dysfunction.JCI insight · 2018Article
- Danger signals from mitochondrial DAMPS in trauma and post-injury sepsis.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018Review
- Innate immune responses to trauma.Nature immunology · 2018Review
- High Tidal Volume Induces Mitochondria Damage and Releases Mitochondrial DNA to Aggravate the Ventilator-Induced Lung Injury.Frontiers in immunology · 2018Article
- Peritoneal cavity lavage reduces the presence of mitochondrial damage associated molecular patterns in open abdomen patients.The journal of trauma and acute care surgery · 2017Observational
- Ly6G+ neutrophil-derived miR-223 inhibits the NLRP3 inflammasome in mitochondrial DAMP-induced acute lung injury.Cell death & disease · 2017Article
- Mitochondrial DNA Damage Initiates Acute Lung Injury and Multi-Organ System Failure Evoked in Rats by Intra-Tracheal Pseudomonas Aeruginosa.Shock (Augusta, Ga.) · 2017Article
- Intratracheal instillation of neutrophils rescues bacterial overgrowth initiated by trauma damage-associated molecular patterns.The journal of trauma and acute care surgery · 2017Article
- Fracture initiates systemic inflammatory response syndrome through recruiting polymorphonuclear leucocytes.Immunologic research · 2016Article
- The acute respiratory distress syndrome: from mechanism to translation.Journal of immunology (Baltimore, Md. : 1950) · 2015Review
- Mitochondrial damage-associated molecular patterns from fractures suppress pulmonary immune responses via formyl peptide receptors 1 and 2.The journal of trauma and acute care surgery · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHistorically, fever, pneumonia, and sepsis after trauma are ascribed to pain and poor pulmonary toilet. No evidence supports that assertion however, and no known biologic mechanisms link injury to infection. Our studies show that injured tissues release mitochondria (MT). Mitochondrial damage-associated molecular patterns (mtDAMPs) however can mimic bacterial pathogen-associated danger molecules and attract neutrophils (PMN). We hypothesized that mtDAMPs from traumatized tissue divert neutrophils from the lung, causing susceptibility to infection.
methodsAnesthetized rats (6-10 per group) underwent pulmonary contusion (PC) by chest percussion. When modeling traumatic MT release, some rats had MT isolated from the liver (equal to 5% liver necrosis) injected intraperitoneally (IPMT). Negative controls had PC plus buffer intraperitoneally. Positive controls underwent PC plus cecal ligation and puncture. At 16 hours, bronchoalveolar and peritoneal lavages were performed. Bronchoalveolar lavage fluid (BALF) and peritoneal lavage fluid were assayed for PMN count, albumin, interleukin β, (IL-β), and CINC-1. Assays were normalized to blood urea nitrogen to calculate absolute concentrations.
resultsPC caused alveolar IL-1β and CINC production and a 34-fold increase in BALF neutrophils. As expected, IPMT increased peritoneal IL-1β and CINC and attracted PMN to the abdomen. However, remarkably, IPMT after PC attenuated BALF cytokine accumulation and decreased BALF PMN. Cecal ligation and puncture had no direct effect on BALF PMNs but, like IPMT, blunted BALF leukocytosis after PC.
conclusionRather than acting as a "second hit" to enhance PMN-mediated lung injury, mtDAMPs from trauma and pathogen-associated danger molecules from peritoneal infection diminish PMN accumulation in a contused lung. This may make the lung susceptible to pneumonia. This paradigm provides a novel mechanistic model of the relationship among blunt tissue trauma, systemic inflammation, and pneumonia that can be studied to improve trauma outcomes.
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