Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection
The heat shock protein (HSP) 70.1 gene lies on mouse chromosome 17 among the candidates for Tir1, the major quantitative trait locus associated with response to Trypanosoma congolense infection. To evaluate whether the HSP70.1 gene is involved in the response, we compared the susceptibility of HSP70.1-deficient C57BL/6 J, resistant wild-type C57BL/6 J and susceptible A/J mice. No differences were observed between HSP70.1-deficient and wild-type C57BL/6 J mice in survival time, levels of parasitemia and anemia, suggesting that there is no involvement of the HSP70.1 gene in control of T. congolense infection. The course of infection was markedly different between A/J and C57BL/6 J mice. A/J mice showed a bi-phasic survival pattern, which seemed to be associated with two waves of high parasitemia, but developed only moderate anemia. C57BL/6 J mice controlled parasitemia well but developed severe anemia in the late stage of infection.
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2003-06
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Subjects: | animal diseases, genetics, |
Online Access: | https://hdl.handle.net/10568/1553 https://doi.org/10.1007/s00436-003-0844-3 |
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dig-cgspace-10568-15532023-12-08T19:36:04Z Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection Nakamura, Y. Naessens, Jan Takata, M. Taniguchi, T. Sekikawa, K. Gibson, John P. Iraqi, F.A. animal diseases genetics The heat shock protein (HSP) 70.1 gene lies on mouse chromosome 17 among the candidates for Tir1, the major quantitative trait locus associated with response to Trypanosoma congolense infection. To evaluate whether the HSP70.1 gene is involved in the response, we compared the susceptibility of HSP70.1-deficient C57BL/6 J, resistant wild-type C57BL/6 J and susceptible A/J mice. No differences were observed between HSP70.1-deficient and wild-type C57BL/6 J mice in survival time, levels of parasitemia and anemia, suggesting that there is no involvement of the HSP70.1 gene in control of T. congolense infection. The course of infection was markedly different between A/J and C57BL/6 J mice. A/J mice showed a bi-phasic survival pattern, which seemed to be associated with two waves of high parasitemia, but developed only moderate anemia. C57BL/6 J mice controlled parasitemia well but developed severe anemia in the late stage of infection. 2003-06 2010-05-18T20:45:43Z 2010-05-18T20:45:43Z Journal Article Nakamura, Y.; Naessens, J.; Takata, M.; Taniguchi, T.; Sekikawa, K.; Gibson, J.; Iraqi, F. 2003. Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection. Parasitological Research 90(2):171-174. 0932-0113 1432-1955 https://hdl.handle.net/10568/1553 https://doi.org/10.1007/s00436-003-0844-3 en Copyrighted; all rights reserved Limited Access p. 171-174 Springer Parasitology Research |
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animal diseases genetics animal diseases genetics Nakamura, Y. Naessens, Jan Takata, M. Taniguchi, T. Sekikawa, K. Gibson, John P. Iraqi, F.A. Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection |
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The heat shock protein (HSP) 70.1 gene lies on mouse chromosome 17 among the candidates for Tir1, the major quantitative trait locus associated with response to Trypanosoma congolense infection. To evaluate whether the HSP70.1 gene is involved in the response, we compared the susceptibility of HSP70.1-deficient C57BL/6 J, resistant wild-type C57BL/6 J and susceptible A/J mice. No differences were observed between HSP70.1-deficient and wild-type C57BL/6 J mice in survival time, levels of parasitemia and anemia, suggesting that there is no involvement of the HSP70.1 gene in control of T. congolense infection. The course of infection was markedly different between A/J and C57BL/6 J mice. A/J mice showed a bi-phasic survival pattern, which seemed to be associated with two waves of high parasitemia, but developed only moderate anemia. C57BL/6 J mice controlled parasitemia well but developed severe anemia in the late stage of infection. |
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Journal Article |
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animal diseases genetics |
author |
Nakamura, Y. Naessens, Jan Takata, M. Taniguchi, T. Sekikawa, K. Gibson, John P. Iraqi, F.A. |
author_facet |
Nakamura, Y. Naessens, Jan Takata, M. Taniguchi, T. Sekikawa, K. Gibson, John P. Iraqi, F.A. |
author_sort |
Nakamura, Y. |
title |
Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection |
title_short |
Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection |
title_full |
Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection |
title_fullStr |
Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection |
title_full_unstemmed |
Susceptibility of heat shock protein 70.1-deficient C57BL/6 J, wild-type C57BL/6 J and A/J mice to Trypanosoma congolense infection |
title_sort |
susceptibility of heat shock protein 70.1-deficient c57bl/6 j, wild-type c57bl/6 j and a/j mice to trypanosoma congolense infection |
publisher |
Springer |
publishDate |
2003-06 |
url |
https://hdl.handle.net/10568/1553 https://doi.org/10.1007/s00436-003-0844-3 |
work_keys_str_mv |
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