RESEARCH PAPER
Evidence of Babesia microti penetration of hepatocytes based on in vitro and in vivo studies
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1
Department of Medical Sciences, Wladyslaw Bieganski Collegium Medicum Jan Dlugosz University, Częstochowa, Poland
2
State Sanitary Inspection, Provincial Sanitary and Epidemiological Station, Katowice, Poland
3
Institute of Biology, Biotechnology and Environmental Protection, Faculty of Natural Sciences, University of Silesia, Katowice, Poland
4
Department of Laryngology, Faculty of Medical Sciences in Katowice, Medical University of Silesia in Katowice, Katowice, Poland
5
Department of Small Livestock Breeding, National Research Institute of Animal Production, Kraków, Poland
6
Department of Biotechnology and Nutrigenomics, Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Jastrzębiec, Poland
Corresponding author
Krzysztof Niemczuk
Biotechnology and Nutrigenomic, Institute of Genetics and Animal Biotechnology of the Polish Academy of Sciences, Postępu, 05-552, Magdalenka, Poland
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ABSTRACT
Introduction and objective:
Babesiosis is a tick-borne disease of animals and humans caused by the intraerythrocytic protozoa Babesia genus. The objective of this study was to demonstrate that B. microti can invade not only blood cells but also cells of other parenchymal organs, and to examine the effects of this parasitemia. An additional objective was to ascertain whether there were differences in the response of B. microti to hepatocytes in vitro and in vivo conditions.
Material and methods:
Wistar rats and the reference hepatocyte cell line Clone 9 isolated from rat livers were used. The rats and cell cultures were infected with an inoculum of B. microti. The investigation of cells in vitro and tissues in vivo was conducted using a light microscope, transmission electron microscope, atomic force microscope, and molecular methods.
Results:
The research findings revealed substantial structural damage to cells, including hydropic degeneration and mitochondrial swelling in B. microti-infected hepatocytes under culture conditions. Similar damage to hepatocytes and thrombosis formation in liver blood vessels were observed. These changes indicated severe liver dysfunction and inflammation of the liver.
Conclusions:
B. microti in intermediate hosts can infect erythrocytes, lymphocytes, and other cells, such as hepatocytes. B. microti affects liver cells directly in in vitro conditions and causes significant liver dysfunction in infected animals. The observed alterations in the blood vessels, including the adhesion of erythrocytes and thrombocytes to the vessel endothelium, provided compelling evidence that the infection of the intermediate host, B. microti, results in haemodynamic disturbances that significantly impact liver dysfunction.
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