@article{oai:jichi-ir.repo.nii.ac.jp:00001022,
 author = {Shimada, Mizuho and Hayakawa, H. Eri and Matsuoka, Hiroyuki},
 journal = {自治医科大学紀要, Jichi Medical University Journal},
 month = {Mar},
 note = {Malaria parasites grow in erythrocytes, while the important symptoms reflecting disease severity are observed in the brain and/or the gastrointestinal (GI) tract in human and murine malaria. Plasmodium
berghei ANKA (PbA-) is widely used as an experimental model to cause lethal murine malaria. We previously reported GI pathophysiology with weight loss on PbA-C57BL/6 mice. Accordingly, we hypothesized that mitigation of weight loss might help ameliorate GI pathophysiology on PbA-C57BL/6 mice. This study aimed to investigate whether administration of heat-killed Lactobacillus sakei HS-1 (HK LS HS-1), a newly identified influencing weight gain on healthy domestic animals, mitigates weight loss and/ or GI pathophysiology on PbA-C57BL/6 mice.
Six C57BL/6 mice were infected with P. berghei-ANKA strain via infective mosquitoes. Thereafter, half of the mice were randomly assigned to receive HK LS HS-1 from day zero until the day of dissection on day 8. Disease states in mice with and without HK LS HS-1 were compared with respect to weight change, food intake, and GI pathophysiology. This experiment was performed three sets.
Overall, the weight (%) was higher in the HK LS HS-1 group than in the control group (p = 0.001), while the food intake (g) was comparable in both the groups. Further, pathological changes of the small intestine did not occur in the HK LS HS-1 group.},
 pages = {13--19},
 title = {Heat-killed Lactobacillus sakei HS-1 mitigates small intestinal pathophysiology on Plasmodium berghei ANKA infected C57BL/6 mice},
 volume = {43},
 year = {2021}
}