Onset of hepatic erythropoiesis after malarial infection in mice.
Plasmodium yoelii-infected erythrocytes were injected into mice with or without 6.5 Gy irradiation. This irradiation suppressed erythropoiesis and induced severe immunosuppression. However, these mice showed a rather delayed infection, suggesting that fresh erythrocytes may become malarial targets. In other words, malarial infection did not persist without newly generated erythrocytes in mice. We then examined erythropoiesis in the liver and bone marrow of mice with malaria. Surprisingly, erythropoiesis began in the liver. At this time, the serum level of erythropoietin (EPO) was prominently elevated and the EPO mRNA also became detectable in the kidney. Many clusters of red blood cells appeared de novo in the parenchymal space of the liver. These results revealed that malarial infection had a potential to induce the onset of hepatic erythropoiesis in mice.
Halder
Ramesh C
RC
Department of Immunology, Niigata University School of Medicine, Niigata 951-8510, Japan.
Abe
Tetsuya
T
Mannoor
M Kaiissar
MK
Morshed
Sufi Reza M
SR
Ariyasinghe
Anoja
A
Watanabe
Hisami
H
Kawamura
Hiroki
H
Sekikawa
Hiroho
H
Hamada
Hiromasa
H
Nishiyama
Yasuhiro
Y
Ishikawa
Hiromichi
H
Toba
Ken
K
Abo
Toru
T
D000818:Animals; D004195:Disease Models, Animal; D004920:Erythropoiesis / Q000502:physiology*; D007150:Immunohistochemistry; D007963:Leukocytes, Mononuclear / Q000502:physiology; D008099:Liver / Q000473:pathology / Q000503:physiopathology*; D008288:Malaria / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018512:Parasitemia / Q000276:immunology / Q000503:physiopathology; D010967:Plasmodium yoelii; D012016:Reference Values; D013997:Time Factors