Lilliehöök, Inger
- Department of Clinical Sciences, Swedish University of Agricultural Sciences
Research article2016Peer reviewed
Lilliehöök, Inger; Tvedten, Harold; Bröjer, Johan; Edner, Anna; Nostell, Katarina
Background: Neutrophil myeloperoxidase content is determined by the Advia 2120 hematology system by staining characteristics. Changes in myeloperoxidase staining are shown by location of neutrophils on Advia peroxidase dot plots and as myeloperoxidase index (MPXI). Significant changes in MPXI have been reported during severe inflammation in horses, dogs, and people but conclusions were inconsistent.Objectives: Infusion of endotoxin was used to initiate an inflammatory stimulus under controlled conditions and over a longer time period than in previous studies to document kinetics of changes in neutrophil numbers, morphology, and myeloperoxidase staining. Identification of consistent time-related changes may allow better interpretation of changes in neutrophil characteristics during inflammation.Materials: Five Standardbred trotting horses received an intravenous infusion over a 6-hour period with Escherichia coli endotoxin. Neutrophil count, MPXI, neutrophil characteristics in Advia 2120 Perox dot plots and neutrophil morphology in blood smears were monitored with repeated sampling for up to 10 days.Results: Endotoxin infusion immediately caused severe neutropenia which converted to neutrophilia 14 hours after start of endotoxin infusion. Neutrophilia was still present 78 hours after start of infusion. Large giant neutrophils first appeared in blood smears and Advia Perox dot plots after 36-48 hours. A marked and consistent decrease in MPXI was seen in all horses 6 days (150 hours) after endotoxin exposure.Conclusions: Endotoxemia caused prominent, time-related changes in equine neutrophil characteristics including emergence of giant neutrophils and markedly decreased MPXI several days after endotoxin infusion.
Advia 2120; blood; giant neutrophils; horse; toxic changes, bone marrow, myelopoiesis
Veterinary Clinical Pathology
2016, Volume: 45, number: 1, pages: 66-72 Publisher: WILEY-BLACKWELL
Pathobiology
Clinical Science
DOI: https://doi.org/10.1111/vcp.12334
https://res.slu.se/id/publ/76267