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The histopathological study in C57BL/6 and Swiss Webster mice infected with Plasmodium berghei ANKA | ||
| Archives of Razi Institute | ||
| مقالات آماده انتشار، پذیرفته شده، انتشار آنلاین از تاریخ 27 مهر 1405 اصل مقاله (1.76 M) | ||
| نوع مقاله: Original Articles | ||
| شناسه دیجیتال (DOI): 10.66224/ari.2026.373538.4230 | ||
| نویسندگان | ||
| Putri Reno Intan* 1؛ Yulvian Sani2؛ Sukmayati Alegantina3؛ Sela Septima Mariya1؛ Fitrine Ekawasti2؛ Ratih Rinendyaputri1؛ Hidayatul Fajri1؛ Indah Fajarwati1؛ Salim Arrokhman1؛ Jiro Hasegawa Situmorang1؛ Rita Marleta Dewi3 | ||
| 1Center for Biomedical Research, Research Organization for Health, National Research and Innovation Agency (BRIN), Bogor, West Java, Indonesia | ||
| 2Research Center for Veterinary Science, Research Organization for Health, National Research and Innovation Agency (BRIN), Bogor, West Java, Indonesia | ||
| 3Research Center for Pharmaceutical Ingredients and Traditional Medicine, National Research and Innovation Agency (BRIN), Bogor, West Java, Indonesia | ||
| چکیده | ||
| Introduction: Animal models provide important information regarding the pathogenesis, protection, and diagnosis of various diseases. This study aimed to investigate the histopathological alterations in Plasmodium berghei ANKA (PbA) infection in C57BL/6 and Swiss Webster mice. Materials and Methods: Both mouse strains were used in this study. Fifteen mice of each strain were divided into three groups: (1) positive control group (Group 1) infected with 107 PbA in 200 μl RBC and treated with dihydroartemisinin-piperaquine (DHP); (2) negative control group (Group 2) infected with PbA as previously described and treated with aquadest; and (3) normal group (Group 3) without infection and treated with aquadest. Results: Microscopic examination revealed splenonecrosis, indicated by the depletion of white pulp and megakaryocytes and accumulation of hemosiderin in the spleen; midzonal hepatic degeneration and/or necrosis, followed by infiltration of lymphocytes and macrophages and accumulation of hemosiderin in the liver; pneumonia; and pulmonary edema in the lungs. These lesions were consistently observed in both the mouse strains. Spleen lesions were more severe in Swiss Webster mice than in C57BL/6 mice, whereas hepatic necrosis was more severe in C57BL/6 mice. However, the lung lesions were not significantly different between the two mouse strains, with only mild lesions observed. Conclusions: Our findings revealed strain-dependent differences in organ pathology during Plasmodium berghei ANKA infection. C57BL/6 mice are more prone to hepatic necrosis, whereas Swiss Webster mice exhibit severe splenic damage. These differences clarify the inconsistencies and provide practical guidance for selecting appropriate mouse models for malaria research. | ||
| کلیدواژه‌ها | ||
| Experimental pathology؛ Hemosiderin accumulation؛ Hepatic necrosis؛ Plasmodium؛ Splenomegaly | ||
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