ArticleCritical care medicine2013
Cecal ligation and puncture-induced murine sepsis does not cause lung injury.
Article in Critical care medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Evaluating skeletal muscle dysfunction and recovery in a zymosan model of critical illness in mice.Disease models & mechanisms · 2026Article
- Kidney mitochondrial DNA contributes to systemic IL-6 release in sepsis-associated acute kidney injury.JCI insight · 2025Article
- Inhibition of Farnesoid-x-receptor signaling during abdominal sepsis by dysbiosis exacerbates gut barrier dysfunction.Cell communication and signaling : CCS · 2025Article
- Nanoemulsions and nanocapsules loaded with Melaleuca alternifolia essential oil for sepsis treatment.Drug delivery and translational research · 2024Article
- Translational medicine for acute lung injury.Journal of translational medicine · 2024Review
- A Novel Scoring System for Humane Endpoints in Mice with Cecal Ligation and Puncture-Induced Sepsis.Comparative medicine · 2023Article
- DNases improve effectiveness of antibiotic treatment in murine polymicrobial sepsis.Frontiers in immunology · 2023Article
- A two-hit model of sepsis plus hyperoxia causes lung permeability and inflammation.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- ACE2 Promoted by STAT3 Activation Has a Protective Role in Early-Stage Acute Kidney Injury of Murine Sepsis.Frontiers in medicine · 2022Article
- Endothelial SOCS3 maintains homeostasis and promotes survival in endotoxemic mice.JCI insight · 2021Article
- Impaired angiotensin II type 1 receptor signaling contributes to sepsis-induced acute kidney injury.Kidney international · 2021Article
- Comparison of direct and indirect models of early induced acute lung injury.Intensive care medicine experimental · 2020Article
- 2-Chlorofatty acids are biomarkers of sepsis mortality and mediators of barrier dysfunction in rats.Journal of lipid research · 2020Article
- Sepsis therapies: learning from 30 years of failure of translational research to propose new leads.EMBO molecular medicine · 2020Review
- Hydrocortisone, Ascorbic Acid, and Thiamine (HAT) Therapy Decreases Oxidative Stress, Improves Cardiovascular Function, and Improves Survival in Murine Sepsis.Shock (Augusta, Ga.) · 2020Article
- Long non-coding RNA-HOTAIR promotes the progression of sepsis by acting as a sponge of miR-211 to induce IL-6R expression.Experimental and therapeutic medicine · 2019Article
- Mild Traumatic Brain Injury in Mice Beneficially Alters Lung NK1R and Structural Protein Expression to Enhance Survival after Pseudomonas aeruginosa Infection.The American journal of pathology · 2019Article
- Part II: Minimum Quality Threshold in Preclinical Sepsis Studies (MQTiPSS) for Types of Infections and Organ Dysfunction Endpoints.Shock (Augusta, Ga.) · 2019Review
- Mechanical ventilation enhances extrapulmonary sepsis-induced lung injury: role of WISP1-αvβ5 integrin pathway in TLR4-mediated inflammation and injury.Critical care (London, England) · 2018Article
- Translational Sepsis Research: Spanning the Divide.Critical care medicine · 2018Review
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9 authors.
Funding
Abstract
objectiveThe cause of death in murine models of sepsis remains unclear. The primary purpose of this study was to determine if significant lung injury develops in mice predicted to die after cecal ligation and puncture-induced sepsis compared with those predicted to live.
designProspective, laboratory controlled experiments.
settingUniversity research laboratory. SUBJECTS: Adult, female, outbred Institute of Cancer Research mice.
interventionsMice underwent cecal ligation and puncture to induce sepsis. Two groups of mice were euthanized at 24 and 48 hrs postcecal ligation and puncture and samples were collected. These mice were further stratified into groups predicted to die (Die-P) and predicted to live (Live-P) based on plasma interleukin-6 levels obtained 24 hrs postcecal ligation and puncture. Multiple measures of lung inflammation and lung injury were quantified in these two groups. Results from a group of mice receiving intratracheal normal saline without surgical intervention were also included as a negative control. As a positive control, bacterial pneumonia was induced with Pseudomonas aeruginosa to cause definitive lung injury. Separate mice were followed for survival until Day 28 postcecal ligation and puncture. These mice were used to verify the interleukin-6 cutoffs for survival prediction. MEASUREMENTS AND MAIN
resultsAfter sepsis, both the Die-P and Live-P mice had significantly suppressed measures of respiratory physiology but maintained normal levels of arterial oxygen saturation. Bronchoalveolar lavage levels of pro- and anti-inflammatory cytokines were not elevated in the Die-P mice compared with the Live-P. In addition, there was no increase in the recruitment of neutrophils to the lung, pulmonary vascular permeability, or histological evidence of damage. In contrast, all of these pulmonary injury and inflammatory parameters were increased in mice with Pseudomonas pneumonia.
conclusionsThese data demonstrate that mice predicted to die during sepsis have no significant lung injury. In murine intra-abdominal sepsis, pulmonary injury cannot be considered the etiology of death in the acute phase.
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