ArticleCritical care (London, England)2020
Mode of bacterial killing affects the inflammatory response and associated organ dysfunctions in a porcine E. coli intensive care sepsis model.
Article in Critical care (London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05511129 (Tolerance and Efficacy of Amiklin Administration During Nosocomial Infections Complicating COVID-19 in the ICU), which is not on this map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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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.
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.
Tolerance and Efficacy of Amiklin Administration During Nosocomial Infections Complicating COVID-19 in the ICU
Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Does kidney function in experimental porcine sepsis fulfill the RIFLE criteria for acute kidney injury? A systematic review.Frontiers in physiology · 2026Pooled it
- A Review of Fluoroquinolones with a Focus on Veterinary-Approved Agents.Biomolecules · 2026Review
- Association between early prophylactic heparin therapy and mortality in patients with septic shock secondary to respiratory infections: analysis based on MIMIC-IV database.BMC infectious diseases · 2025Article
- The acute changes in intracellular amino acid production during sepsis do not relate to plasma concentrations.Clinical nutrition (Edinburgh, Scotland) · 2025Article
- An ovine septic shock model of live bacterial infusion.Intensive care medicine experimental · 2024Article
- Evaluation of Bacteriophage Cocktail on Septicemia Caused by Colistin-ResistantFrontiers in pharmacology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis is often treated with penicillin-binding protein 3 (PBP-3) acting β-lactam antibiotics, such as piperacillin-tazobactam, cefotaxime, and meropenem. They cause considerable bacterial structural changes and have in vitro been associated with an increased inflammatory response. In a clinically relevant large animal sepsis model, our primary aim was to investigate whether bacteria killed by a PBP-3-active antibiotic has a greater effect on the early inflammatory response and organ dysfunction compared with corresponding amounts of live or heat-killed bacteria. A secondary aim was to determine whether the addition of an aminoglycoside could mitigate the cefuroxime-induced response.
methodKilled or live Escherichia coli were administrated as a 3-h infusion to 16 healthy pigs in a prospective, randomized controlled interventional experimental study. Cefuroxime was chosen as the PBP-3-active antibiotic and tobramycin represented the aminoglycosides. The animals were randomized to receive (I) bacteria killed by cefuroxime, (II) live bacteria, (III) bacteria killed by heat, or (IV) bacteria killed by the combination of cefuroxime and tobramycin. Plasma endotoxin, tumor necrosis factor alpha, interleukin-6, interleukin-10, leukocytes, and organ function were recorded at the start of the experiment and then hourly for 6 h.
resultsDifferences in dynamics of concentration over time between the four treatment groups were found for the three cytokines (p < 0.001). Animals receiving cefuroxime-killed bacteria demonstrated higher responses than those receiving live (p < 0.05) or heat-killed bacteria (p < 0.01). The addition of tobramycin reduced the cefuroxime-induced responses (p < 0.001). The cytokine responses were associated with leucocyte activation that was further associated with pulmonary dysfunction and increases in lactate (p < 0.01).
conclusionsIn comparison with live or heat-killed bacteria, bacteria killed by a PBP-3-active antibiotic induced an increased inflammatory response that appears to be associated with deteriorated organ and cellular function. The addition of an aminoglycoside to the PBP-3-active antibiotic reduced that response.
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