Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis

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Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis. / Amin, Daniel N; Rottenberg, Martin E; Thomsen, Allan R; Mumba, Dieudonné; Fenger, Christina; Kristensson, Krister; Büscher, Philippe; Finsen, Bente; Masocha, Willias.

In: Journal of Infectious Diseases, Vol. 200, No. 10, 2009, p. 1556-65.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Amin, DN, Rottenberg, ME, Thomsen, AR, Mumba, D, Fenger, C, Kristensson, K, Büscher, P, Finsen, B & Masocha, W 2009, 'Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis', Journal of Infectious Diseases, vol. 200, no. 10, pp. 1556-65. https://doi.org/10.1086/644597

APA

Amin, D. N., Rottenberg, M. E., Thomsen, A. R., Mumba, D., Fenger, C., Kristensson, K., Büscher, P., Finsen, B., & Masocha, W. (2009). Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis. Journal of Infectious Diseases, 200(10), 1556-65. https://doi.org/10.1086/644597

Vancouver

Amin DN, Rottenberg ME, Thomsen AR, Mumba D, Fenger C, Kristensson K et al. Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis. Journal of Infectious Diseases. 2009;200(10):1556-65. https://doi.org/10.1086/644597

Author

Amin, Daniel N ; Rottenberg, Martin E ; Thomsen, Allan R ; Mumba, Dieudonné ; Fenger, Christina ; Kristensson, Krister ; Büscher, Philippe ; Finsen, Bente ; Masocha, Willias. / Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis. In: Journal of Infectious Diseases. 2009 ; Vol. 200, No. 10. pp. 1556-65.

Bibtex

@article{0e8fd0b01ca211df8ed1000ea68e967b,
title = "Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis",
abstract = "BACKGROUND: Human African trypanosomiasis, caused by Trypanosoma brucei, involves an early hemolymphatic stage followed by a late encephalitic stage. METHODS: We studied the expression of chemokines with use of microarray and enzyme-linked immunosorbent assay in T. brucei brucei-infected mice and in patients with human African trypanosomiasis and examined their role in controlling brain accumulation of T cells and parasites. RESULTS: The messenger RNAs (mRNAs) encoding CXCR3 ligands CXCL9 and CXCL10 demonstrated the greatest increases among chemokines in brain specimens of infected mice, as determined by microarray. CXCL9 and CXCL10 mRNA accumulation was interferon (IFN)-gamma-dependent. Expression of CXCL10 was predominantly observed in astrocytes. Weight loss was registered in wild-type but not in CXCL10(-/-) and CXCR3(-/-) infected mice. Infected CXCL10(-/-) or CXCR3(-/-) mice demonstrated reduced accumulation of trypanosomes and T cells in the brain parenchyma but similar parasitemia levels, compared with wild-type mice. CXCL10 and IFN-gamma levels were increased in the cerebrospinal fluid of patients with late stage but not early stage human African trypanosomiasis. Levels of CXCL10 in patients with late stage human African trypanosomiasis were associated with somnolence, low body weight, and trypanosomes in the cerebrospinal fluid. CONCLUSION: IFN-gamma-dependent CXCL10 is critical for accumulation of T cells and trypanosomes in the brain during experimental African trypanosomiasis. Data suggest CXCL10 as a candidate marker for late stage human African trypanosomiasis.",
author = "Amin, {Daniel N} and Rottenberg, {Martin E} and Thomsen, {Allan R} and Dieudonn{\'e} Mumba and Christina Fenger and Krister Kristensson and Philippe B{\"u}scher and Bente Finsen and Willias Masocha",
note = "Keywords: Animals; Astrocytes; Chemokine CXCL10; Chemokine CXCL9; Humans; Mice; Mice, Knockout; RNA, Messenger; Receptors, CXCR3; Trypanosoma brucei brucei; Trypanosoma brucei gambiense; Trypanosomiasis, African; Up-Regulation",
year = "2009",
doi = "10.1086/644597",
language = "English",
volume = "200",
pages = "1556--65",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "10",

}

RIS

TY - JOUR

T1 - Expression and role of CXCL10 during the encephalitic stage of experimental and clinical African trypanosomiasis

AU - Amin, Daniel N

AU - Rottenberg, Martin E

AU - Thomsen, Allan R

AU - Mumba, Dieudonné

AU - Fenger, Christina

AU - Kristensson, Krister

AU - Büscher, Philippe

AU - Finsen, Bente

AU - Masocha, Willias

N1 - Keywords: Animals; Astrocytes; Chemokine CXCL10; Chemokine CXCL9; Humans; Mice; Mice, Knockout; RNA, Messenger; Receptors, CXCR3; Trypanosoma brucei brucei; Trypanosoma brucei gambiense; Trypanosomiasis, African; Up-Regulation

PY - 2009

Y1 - 2009

N2 - BACKGROUND: Human African trypanosomiasis, caused by Trypanosoma brucei, involves an early hemolymphatic stage followed by a late encephalitic stage. METHODS: We studied the expression of chemokines with use of microarray and enzyme-linked immunosorbent assay in T. brucei brucei-infected mice and in patients with human African trypanosomiasis and examined their role in controlling brain accumulation of T cells and parasites. RESULTS: The messenger RNAs (mRNAs) encoding CXCR3 ligands CXCL9 and CXCL10 demonstrated the greatest increases among chemokines in brain specimens of infected mice, as determined by microarray. CXCL9 and CXCL10 mRNA accumulation was interferon (IFN)-gamma-dependent. Expression of CXCL10 was predominantly observed in astrocytes. Weight loss was registered in wild-type but not in CXCL10(-/-) and CXCR3(-/-) infected mice. Infected CXCL10(-/-) or CXCR3(-/-) mice demonstrated reduced accumulation of trypanosomes and T cells in the brain parenchyma but similar parasitemia levels, compared with wild-type mice. CXCL10 and IFN-gamma levels were increased in the cerebrospinal fluid of patients with late stage but not early stage human African trypanosomiasis. Levels of CXCL10 in patients with late stage human African trypanosomiasis were associated with somnolence, low body weight, and trypanosomes in the cerebrospinal fluid. CONCLUSION: IFN-gamma-dependent CXCL10 is critical for accumulation of T cells and trypanosomes in the brain during experimental African trypanosomiasis. Data suggest CXCL10 as a candidate marker for late stage human African trypanosomiasis.

AB - BACKGROUND: Human African trypanosomiasis, caused by Trypanosoma brucei, involves an early hemolymphatic stage followed by a late encephalitic stage. METHODS: We studied the expression of chemokines with use of microarray and enzyme-linked immunosorbent assay in T. brucei brucei-infected mice and in patients with human African trypanosomiasis and examined their role in controlling brain accumulation of T cells and parasites. RESULTS: The messenger RNAs (mRNAs) encoding CXCR3 ligands CXCL9 and CXCL10 demonstrated the greatest increases among chemokines in brain specimens of infected mice, as determined by microarray. CXCL9 and CXCL10 mRNA accumulation was interferon (IFN)-gamma-dependent. Expression of CXCL10 was predominantly observed in astrocytes. Weight loss was registered in wild-type but not in CXCL10(-/-) and CXCR3(-/-) infected mice. Infected CXCL10(-/-) or CXCR3(-/-) mice demonstrated reduced accumulation of trypanosomes and T cells in the brain parenchyma but similar parasitemia levels, compared with wild-type mice. CXCL10 and IFN-gamma levels were increased in the cerebrospinal fluid of patients with late stage but not early stage human African trypanosomiasis. Levels of CXCL10 in patients with late stage human African trypanosomiasis were associated with somnolence, low body weight, and trypanosomes in the cerebrospinal fluid. CONCLUSION: IFN-gamma-dependent CXCL10 is critical for accumulation of T cells and trypanosomes in the brain during experimental African trypanosomiasis. Data suggest CXCL10 as a candidate marker for late stage human African trypanosomiasis.

U2 - 10.1086/644597

DO - 10.1086/644597

M3 - Journal article

C2 - 19827943

VL - 200

SP - 1556

EP - 1565

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 10

ER -

ID: 18081405