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Intensive Care Med Exp. 2019 Jul 25;7(Suppl 1):47. doi: 10.1186/s40635-019-0261-2.

Development of a model for anemia of inflammation that is relevant to critical care.

Author information

1
Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, Amsterdam, 1105, AZ, the Netherlands. m.boshuizen@amc.nl.
2
Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, 1066, CX, The Netherlands. m.boshuizen@amc.nl.
3
Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, 1066, CX, The Netherlands.
4
Department of Microbiology, Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam, Amsterdam, 1105, AZ, The Netherlands.
5
Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, Amsterdam, 1105, AZ, the Netherlands.
6
Department of Pulmonary and Critical Care Medicine, Thorax Institute, Hospital Clínic, 08036, Barcelona, Spain.
7
Department of Surgical Sciences and Integrated Diagnostics (DISC), San Martino Policlinico Hospital - IRCCS for Oncology, 16132, Genova, Italy.

Abstract

BACKGROUND:

Anemia of inflammation (AI) is common in critically ill patients. Although this syndrome negatively impacts the outcome of critical illness, understanding of its pathophysiology is limited. Also, new therapies that increase iron availability for erythropoiesis during AI are upcoming. A model of AI induced by bacterial infections that are relevant for the critically ill is currently not available. This paper describes the development of an animal model for AI that is relevant for critical care research.

RESULTS:

In experiments with rats, the rats were inoculated either repeatedly or with a slow release of Streptococcus pneumoniae or Pseudomonas aeruginosa. Rats became ill, but their hemoglobin levels remained stable. The use of a higher dose of bacteria resulted in a lethal model. Then, we turned to a model with longer disease duration, using pigs that were supported by mechanical ventilation after inoculation with P. aeruginosa. The pigs became septic 12 to 24 h after inoculation, with a statistically significant decrease in mean arterial pressure and base excess, while heart rate tended to increase. Pigs needed resuscitation and vasopressor therapy to maintain a mean arterial pressure > 60 mmHg. After 72 h, the pigs developed anemia (baseline 9.9 g/dl vs. 72 h, 7.6 g/dl, p = 0.01), characterized by statistically significant decreased iron levels, decreased transferrin saturation, and increased ferritin. Hepcidin levels tended to increase and transferrin levels tended to decrease.

CONCLUSIONS:

Using pathogens commonly involved in pulmonary sepsis, AI could not be induced in rats. Conversely, in pigs, P. aeruginosa induced pulmonary sepsis with concomitant AI. This AI model can be applied to study the pathophysiology of AI in the critically ill and to investigate the effectivity and toxicity of new therapies that aim to increase iron availability.

KEYWORDS:

Anemia of inflammation; Animal model; ICU; Infection; Iron

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