Anemia amelioration by lactose infusion during trypanosomosis could be associated with erythrocytes membrane de-galactosylation.
African trypanosomosis is a potentially fatal disease that is caused by extracellular parasitic protists known as African trypanosomes. These parasites inhabit the blood stream of their mammalian hosts and produce a number of pathological features, amongst which is anemia. Etiology of the anemia has been partly attributed to an autoimmunity-like mediated erythrophagocytosis of de-sialylated red blood cells (dsRBCs) by macrophages. Lactose infusion to infected animals has proven effective at delaying progression of the anemia. However, the mechanism of this anemia prevention is yet to be well characterized. Here, the hypothesis of a likely induced further modification of the dsRBCs was investigated. RBC membrane galactose (RBC m-GAL) and packed cell volume (PCV) were measured during the course of experimental trypanosomosis in mice infected with Trypanosoma congolense (stb 212). Intriguingly, while the membrane galactose on the RBCs of infected and lactose-treated mice (group D) decreased as a function of parasitemia, that of the lactose-untreated infected group (group C) remained relatively constant, as was recorded for the uninfected lactose-treated control (group B) animals. At the peak of infection, the respective cumulative percent decrease in PCV and membrane galactose were 30 and 185 for group D, and 84 and 13 for group C. From this observed inverse relationship between RBCs membrane galactose and PCV, it is logical to rationalize that the delay of anemia progression during trypanosomosis produced by lactose might have resulted from an induction of galactose depletion from dsRBCs, thereby preventing their recognition by the macrophages.
Department of Biochemistry, Ahmadu Bello University, Zaria 2222, Nigeria; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan; Department of Applied Biology, Graduate School of Science and Technology, Kyoto Institute of Technology, Sakyo-ku, Kyoto 606-8585, Japan. Electronic address: balogun1@m.u-tokyo.ac.jp.
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Balogun
Department of Biological Sciences, Federal University Dutse, P.M.B. 7156, Dutse, Jigawa State, Nigeria.
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Balogun
Department of Physiology, Faculty of Biomedical Sciences, Kampala International University, Uganda.
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Yusuf
Department of Biochemistry, Ahmadu Bello University, Zaria 2222, Nigeria.
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Inuwa
Department of Biological Sciences, Ahmadu Bello University, Zaria 2222, Nigeria.
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Ndams
Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
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Sheridan
Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
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Inaoka
Department of Applied Biology, Graduate School of Science and Technology, Kyoto Institute of Technology, Sakyo-ku, Kyoto 606-8585, Japan.
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Shiba
Department of Applied Biology, Graduate School of Science and Technology, Kyoto Institute of Technology, Sakyo-ku, Kyoto 606-8585, Japan.
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Harada
Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
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Kita
Department of Veterinary Pathology and Microbiology, Ahmadu Bello University, Zaria 2222, Nigeria.
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Esievo
Department of Biochemistry, Ahmadu Bello University, Zaria 2222, Nigeria.
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D000740:Anemia / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology; D000818:Animals; D000977:Antiparasitic Agents / Q000494:pharmacology / Q000627:therapeutic use; D004910:Erythrocyte Membrane / Q000187:drug effects* / Q000378:metabolism*; D005690:Galactose / Q000378:metabolism*; D006400:Hematocrit; D007785:Lactose / Q000494:pharmacology* / Q000627:therapeutic use; D051379:Mice; D018512:Parasitemia / Q000473:pathology; D014352:Trypanosomiasis / Q000473:pathology*
D000977:Antiparasitic Agents; D007785:Lactose; D005690:Galactose
Anemia; RBC membrane galactose; Sialidase; Trypanosomosis