Mechanisms controlling anaemia in Trypanosoma congolense infected miceCitation formats

  • External authors:
  • Harry A. Noyes
  • Mohammad H. Alimohammadian
  • Morris Agaba
  • Helmut Fuchs
  • Valerie Gailus-Durner
  • Helen Hulme
  • Fuad Iraqi
  • Stephen Kemp
  • Birgit Rathkolb
  • Eckard Wolf
  • Martin Hrabé de Angelis
  • Delnaz Roshandel
  • Jan Naessens

Standard

Mechanisms controlling anaemia in Trypanosoma congolense infected mice. / Noyes, Harry A.; Alimohammadian, Mohammad H.; Agaba, Morris; Brass, Andy; Fuchs, Helmut; Gailus-Durner, Valerie; Hulme, Helen; Iraqi, Fuad; Kemp, Stephen; Rathkolb, Birgit; Wolf, Eckard; de Angelis, Martin Hrabé; Roshandel, Delnaz; Naessens, Jan.

In: PLoS ONE, Vol. 4, No. 4, e5170, 13.04.2009.

Research output: Contribution to journalArticlepeer-review

Harvard

Noyes, HA, Alimohammadian, MH, Agaba, M, Brass, A, Fuchs, H, Gailus-Durner, V, Hulme, H, Iraqi, F, Kemp, S, Rathkolb, B, Wolf, E, de Angelis, MH, Roshandel, D & Naessens, J 2009, 'Mechanisms controlling anaemia in Trypanosoma congolense infected mice', PLoS ONE, vol. 4, no. 4, e5170. https://doi.org/10.1371/journal.pone.0005170

APA

Noyes, H. A., Alimohammadian, M. H., Agaba, M., Brass, A., Fuchs, H., Gailus-Durner, V., Hulme, H., Iraqi, F., Kemp, S., Rathkolb, B., Wolf, E., de Angelis, M. H., Roshandel, D., & Naessens, J. (2009). Mechanisms controlling anaemia in Trypanosoma congolense infected mice. PLoS ONE, 4(4), [e5170]. https://doi.org/10.1371/journal.pone.0005170

Vancouver

Noyes HA, Alimohammadian MH, Agaba M, Brass A, Fuchs H, Gailus-Durner V et al. Mechanisms controlling anaemia in Trypanosoma congolense infected mice. PLoS ONE. 2009 Apr 13;4(4). e5170. https://doi.org/10.1371/journal.pone.0005170

Author

Noyes, Harry A. ; Alimohammadian, Mohammad H. ; Agaba, Morris ; Brass, Andy ; Fuchs, Helmut ; Gailus-Durner, Valerie ; Hulme, Helen ; Iraqi, Fuad ; Kemp, Stephen ; Rathkolb, Birgit ; Wolf, Eckard ; de Angelis, Martin Hrabé ; Roshandel, Delnaz ; Naessens, Jan. / Mechanisms controlling anaemia in Trypanosoma congolense infected mice. In: PLoS ONE. 2009 ; Vol. 4, No. 4.

Bibtex

@article{67f720d9b3f9494eb0157ef2afe99556,
title = "Mechanisms controlling anaemia in Trypanosoma congolense infected mice",
abstract = "Background: Trypanosoma congolense are extracellular protozoan parasites of the blood stream of artiodactyls and are one of the main constraints on cattle production in Africa. In cattle, anaemia is the key feature of disease and persists after parasitaemia has declined to low or undetectable levels, but treatment to clear the parasites usually resolves the anaemia. Methodology/Principal Findings: The progress of anaemia after Trypanosoma congolense infection was followed in three mouse strains. Anaemia developed rapidly in all three strains until the peak of the first wave of parasitaemia. This was followed by a second phase, characterized by slower progress to severe anaemia in C57BL/6, by slow recovery in surviving A/J and a rapid recovery in BALB/c. There was no association between parasitaemia and severity of anaemia. Furthermore, functional T lymphocytes are not required for the induction of anaemia, since suppression of T cell activity with Cyclosporin A had neither an effect on the course of infection nor on anaemia. Expression of genes involved in erythropoiesis and iron metabolism was followed in spleen, liver and kidney tissues in the three strains of mice using microarrays. There was no evidence for a response to erythropoietin, consistent with anaemia of chronic disease, which is erythropoietin insensitive. However, the expression of transcription factors and genes involved in erythropoiesis and haemolysis did correlate with the expression of the inflammatory cytokines Il6 and Ifng. Conclusions/Significance: The innate immune response appears to be the major contributor to the inflammation associated with anaemia since suppression of T cells with CsA had no observable effect. Several transcription factors regulating haematopoiesis, Tal1, Gata1, Zfpm1 and Klf1 were expressed at consistently lower levels in C57BL/6 mice suggesting that these mice have a lower haematopoietic capacity and therefore less ability to recover from haemolysis induced anaemia after infection. {\textcopyright} 2009 Noyes et al.",
author = "Noyes, {Harry A.} and Alimohammadian, {Mohammad H.} and Morris Agaba and Andy Brass and Helmut Fuchs and Valerie Gailus-Durner and Helen Hulme and Fuad Iraqi and Stephen Kemp and Birgit Rathkolb and Eckard Wolf and {de Angelis}, {Martin Hrab{\'e}} and Delnaz Roshandel and Jan Naessens",
note = "GR066764MA, Wellcome Trust, United Kingdom",
year = "2009",
month = apr,
day = "13",
doi = "10.1371/journal.pone.0005170",
language = "English",
volume = "4",
journal = "PL o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "4",

}

RIS

TY - JOUR

T1 - Mechanisms controlling anaemia in Trypanosoma congolense infected mice

AU - Noyes, Harry A.

AU - Alimohammadian, Mohammad H.

AU - Agaba, Morris

AU - Brass, Andy

AU - Fuchs, Helmut

AU - Gailus-Durner, Valerie

AU - Hulme, Helen

AU - Iraqi, Fuad

AU - Kemp, Stephen

AU - Rathkolb, Birgit

AU - Wolf, Eckard

AU - de Angelis, Martin Hrabé

AU - Roshandel, Delnaz

AU - Naessens, Jan

N1 - GR066764MA, Wellcome Trust, United Kingdom

PY - 2009/4/13

Y1 - 2009/4/13

N2 - Background: Trypanosoma congolense are extracellular protozoan parasites of the blood stream of artiodactyls and are one of the main constraints on cattle production in Africa. In cattle, anaemia is the key feature of disease and persists after parasitaemia has declined to low or undetectable levels, but treatment to clear the parasites usually resolves the anaemia. Methodology/Principal Findings: The progress of anaemia after Trypanosoma congolense infection was followed in three mouse strains. Anaemia developed rapidly in all three strains until the peak of the first wave of parasitaemia. This was followed by a second phase, characterized by slower progress to severe anaemia in C57BL/6, by slow recovery in surviving A/J and a rapid recovery in BALB/c. There was no association between parasitaemia and severity of anaemia. Furthermore, functional T lymphocytes are not required for the induction of anaemia, since suppression of T cell activity with Cyclosporin A had neither an effect on the course of infection nor on anaemia. Expression of genes involved in erythropoiesis and iron metabolism was followed in spleen, liver and kidney tissues in the three strains of mice using microarrays. There was no evidence for a response to erythropoietin, consistent with anaemia of chronic disease, which is erythropoietin insensitive. However, the expression of transcription factors and genes involved in erythropoiesis and haemolysis did correlate with the expression of the inflammatory cytokines Il6 and Ifng. Conclusions/Significance: The innate immune response appears to be the major contributor to the inflammation associated with anaemia since suppression of T cells with CsA had no observable effect. Several transcription factors regulating haematopoiesis, Tal1, Gata1, Zfpm1 and Klf1 were expressed at consistently lower levels in C57BL/6 mice suggesting that these mice have a lower haematopoietic capacity and therefore less ability to recover from haemolysis induced anaemia after infection. © 2009 Noyes et al.

AB - Background: Trypanosoma congolense are extracellular protozoan parasites of the blood stream of artiodactyls and are one of the main constraints on cattle production in Africa. In cattle, anaemia is the key feature of disease and persists after parasitaemia has declined to low or undetectable levels, but treatment to clear the parasites usually resolves the anaemia. Methodology/Principal Findings: The progress of anaemia after Trypanosoma congolense infection was followed in three mouse strains. Anaemia developed rapidly in all three strains until the peak of the first wave of parasitaemia. This was followed by a second phase, characterized by slower progress to severe anaemia in C57BL/6, by slow recovery in surviving A/J and a rapid recovery in BALB/c. There was no association between parasitaemia and severity of anaemia. Furthermore, functional T lymphocytes are not required for the induction of anaemia, since suppression of T cell activity with Cyclosporin A had neither an effect on the course of infection nor on anaemia. Expression of genes involved in erythropoiesis and iron metabolism was followed in spleen, liver and kidney tissues in the three strains of mice using microarrays. There was no evidence for a response to erythropoietin, consistent with anaemia of chronic disease, which is erythropoietin insensitive. However, the expression of transcription factors and genes involved in erythropoiesis and haemolysis did correlate with the expression of the inflammatory cytokines Il6 and Ifng. Conclusions/Significance: The innate immune response appears to be the major contributor to the inflammation associated with anaemia since suppression of T cells with CsA had no observable effect. Several transcription factors regulating haematopoiesis, Tal1, Gata1, Zfpm1 and Klf1 were expressed at consistently lower levels in C57BL/6 mice suggesting that these mice have a lower haematopoietic capacity and therefore less ability to recover from haemolysis induced anaemia after infection. © 2009 Noyes et al.

U2 - 10.1371/journal.pone.0005170

DO - 10.1371/journal.pone.0005170

M3 - Article

C2 - 19365556

VL - 4

JO - PL o S One

JF - PL o S One

SN - 1932-6203

IS - 4

M1 - e5170

ER -