ArticleIntensive care medicine experimental2015
Why do they die? Comparison of selected aspects of organ injury and dysfunction in mice surviving and dying in acute abdominal sepsis.
Article in Intensive care medicine experimental, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 44 citations in OpenAlex.
- Optimization of Preclinical Rodent Research Models of Human Shock: Part One Intra-Abdominal Sepsis.Shock (Augusta, Ga.) · 2026Review
- The poikilothermic hypothesis of sepsis.Critical care (London, England) · 2026Review
- Humanized MISTRG6 Mice: A Relevant Translational Model for Examining Early Bone Marrow Changes in Acute CLP Sepsis.Shock (Augusta, Ga.) · 2026Article
- Contactless body temperature assessment for signalling humane endpoints in a mouse model of sepsis.Animal welfare (South Mimms, England) · 2025Article
- Lung immune incompetency after mild peritoneal sepsis and its partial restoration by type 1 interferon: a mouse model study.Intensive care medicine experimental · 2024Article
- Therapeutic effect of recombinant Echinococcus granulosus antigen B subunit 2 protein on sepsis in a mouse model.Parasites & vectors · 2024Article
- Thermoregulation and survival during sepsis: insights from the cecal ligation and puncture experimental model.Intensive care medicine experimental · 2024Article
- Lethal versus surviving sepsis phenotypes displayed a partly differential regional expression of neurotransmitters and inflammation and did not modify the blood-brain barrier permeability in female CLP mice.Intensive care medicine experimental · 2024Article
- Using weight loss to predict outcome and define a humane endpoint in preclinical sepsis studies.Scientific reports · 2024Article
- Two murine models of sepsis: immunopathological differences between the sexes-possible role of TGFβ1 in female resistance to endotoxemia.Biological research · 2023Article
- From Gut to Blood: Spatial and Temporal Pathobiome Dynamics during Acute Abdominal Murine Sepsis.Microorganisms · 2023Article
- Metabolic Alterations in Sepsis.Journal of clinical medicine · 2021Review
- An Early Myelosuppression in the Acute Mouse Sepsis Is Partly Outcome-Dependent.Frontiers in immunology · 2021Article
- Impact of ambient temperature on inflammation-induced encephalopathy in endotoxemic mice-role of phosphoinositide 3-kinase gamma.Journal of neuroinflammation · 2020Article
- Apoptotic cell therapy for cytokine storm associated with acute severe sepsis.Cell death & disease · 2020Article
- Role of Interleukin-33 inFrontiers in immunology · 2020Article
- Part II: Minimum Quality Threshold in Preclinical Sepsis Studies (MQTiPSS) for Types of Infections and Organ Dysfunction Endpoints.Shock (Augusta, Ga.) · 2019Review
- The Fluctuations of Leukocytes and Circulating Cytokines in Septic Humanized Mice Vary With Outcome.Frontiers in immunology · 2019Article
- Part I: Minimum Quality Threshold in Preclinical Sepsis Studies (MQTiPSS) for Study Design and Humane Modeling Endpoints.Shock (Augusta, Ga.) · 2019Review
- Splenectomy modulates early immuno-inflammatory responses to trauma-hemorrhage and protects mice against secondary sepsis.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 3 countries.
Funding
Abstract
backgroundThe mechanisms of sepsis mortality remain undefined. While there is some evidence of organ damage, it is not clear whether this damage alone is sufficient to cause death. Therefore, we aimed to examine contribution of organ injury/dysfunction to early deaths in the mouse abdominal sepsis.
methodsFemale OF-1 mice underwent either medium-severity cecal ligation and puncture (CLP-Only) or non-lethal CLP-ODam (CLP with cisplatin/carbontetrachloride to induce survivable hepatotoxicity and nephrotoxicity). In the first experiment, blood was collected daily from survivors (SUR; CLP-Only and CLP-ODam groups) or until early death (DIED; CLP-Only). In the second experiment (CLP-Only), early outcome was prospectively predicted based on body temperature (BT) and pairs of mice predicted to survive (P-SUR) and die (P-DIE) were sacrificed post-CLP. The overall magnitude of organ injury/dysfunction was compared in retrospectively and prospectively stratified mice.
resultsAt day 7 post-CLP, survival in CLP-Only was 48%, while CLP-ODam was non-lethal. In CLP-Only mice within 24 h of death, urea increased to 78 (versus 40 mg/dl in SUR), ALT to 166 (vs. 108 U/l), LDH to 739 (vs. 438 U/l) and glucose declined to 43 (vs. 62 mg/dl). In CLP-ODam, hypoglycemia was exacerbated (by 1.5-fold) and ALT and LDH were 20- and 8-fold higher versus DIED (CLP-Only) mice. In CLP-Only, predicted deaths (P-DIE) were preceded by a significant rise only in cystatin C (268 vs. 170 ng/ml in P-SUR) but not in creatinine and troponin I. Respiratory function of mitochondria in the liver and kidney of P-SUR and P-DIE CLP-Only mice was not impaired (vs. controls) and ATP level in organs remained similar among all groups. Histologic injury scores in the liver, kidney, heart and lung showed no major disparities among dying, surviving and control mice.
conclusionsIn CLP-Only mice, although the deregulation of parameters indicative of organ injury/dysfunction was greater in dying versus surviving mice, it never exceeded the changes in surviving CLP-ODam animals, and it was not followed by histopathological damage and/or mitochondrial dysfunction. This shows that interpretation of the contribution of the organ injury/dysfunction to early deaths in the CLP model is not straightforward and depends on the pathophysiological origin of the profiled disturbances.
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.