T-cell responses during Trypanosoma brucei infections in mice deficient in inducible nitric oxide synthase

A E Millar, J Sternberg, C McSharry, X Q Wei, F Y Liew, C M R Turner

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

We have investigated the possibility that nitric oxide (NO) synthesis may affect the course of a trypanosome infection via T-cell responses using mice deficient in inducible NO synthase (iNOS). Parasitemia levels increased at the same rate in both iNOS-deficient homozygous and control heterozygous mice, and peak parasitemia values were the same in both groups. However, the heterozygous mice maintained higher parasitemia levels after the peak of an infection than the homozygous mice due to a decrease in the rate of clearance of parasites. In iNOS-deficient mice there was an increase in the numbers of total CD4(+) cells and activated (interleukin-2 receptor-expressing) CD4(+) cells in infected mice compared with the numbers in uninfected mice. Spleen cells from infected iNOS-deficient mice displayed increased proliferative responses and gamma interferon secretion when stimulated in vitro than those of control mice. These data suggest that NO production depresses T-helper 1-like responses generated during Trypanosoma brucei infections, thus promoting the survival of the parasite.

Original languageEnglish
Pages (from-to)3334-3338
Number of pages5
JournalInfection and Immunity
Volume67
Publication statusPublished - 1999

Keywords

  • INTERLEUKIN-2 RECEPTOR EXPRESSION
  • BLOOD-STREAM FORMS
  • AFRICAN TRYPANOSOMIASIS
  • SUPPRESSOR MACROPHAGES
  • IN-VIVO
  • IMMUNOSUPPRESSION
  • INHIBITION
  • INVITRO
  • CATTLE
  • CONGOLENSE

Cite this

Millar, A. E., Sternberg, J., McSharry, C., Wei, X. Q., Liew, F. Y., & Turner, C. M. R. (1999). T-cell responses during Trypanosoma brucei infections in mice deficient in inducible nitric oxide synthase. Infection and Immunity, 67, 3334-3338.

T-cell responses during Trypanosoma brucei infections in mice deficient in inducible nitric oxide synthase. / Millar, A E ; Sternberg, J ; McSharry, C ; Wei, X Q ; Liew, F Y ; Turner, C M R .

In: Infection and Immunity, Vol. 67, 1999, p. 3334-3338.

Research output: Contribution to journalArticle

Millar, A E ; Sternberg, J ; McSharry, C ; Wei, X Q ; Liew, F Y ; Turner, C M R . / T-cell responses during Trypanosoma brucei infections in mice deficient in inducible nitric oxide synthase. In: Infection and Immunity. 1999 ; Vol. 67. pp. 3334-3338.
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T1 - T-cell responses during Trypanosoma brucei infections in mice deficient in inducible nitric oxide synthase

AU - Millar, A E

AU - Sternberg, J

AU - McSharry, C

AU - Wei, X Q

AU - Liew, F Y

AU - Turner, C M R

PY - 1999

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N2 - We have investigated the possibility that nitric oxide (NO) synthesis may affect the course of a trypanosome infection via T-cell responses using mice deficient in inducible NO synthase (iNOS). Parasitemia levels increased at the same rate in both iNOS-deficient homozygous and control heterozygous mice, and peak parasitemia values were the same in both groups. However, the heterozygous mice maintained higher parasitemia levels after the peak of an infection than the homozygous mice due to a decrease in the rate of clearance of parasites. In iNOS-deficient mice there was an increase in the numbers of total CD4(+) cells and activated (interleukin-2 receptor-expressing) CD4(+) cells in infected mice compared with the numbers in uninfected mice. Spleen cells from infected iNOS-deficient mice displayed increased proliferative responses and gamma interferon secretion when stimulated in vitro than those of control mice. These data suggest that NO production depresses T-helper 1-like responses generated during Trypanosoma brucei infections, thus promoting the survival of the parasite.

AB - We have investigated the possibility that nitric oxide (NO) synthesis may affect the course of a trypanosome infection via T-cell responses using mice deficient in inducible NO synthase (iNOS). Parasitemia levels increased at the same rate in both iNOS-deficient homozygous and control heterozygous mice, and peak parasitemia values were the same in both groups. However, the heterozygous mice maintained higher parasitemia levels after the peak of an infection than the homozygous mice due to a decrease in the rate of clearance of parasites. In iNOS-deficient mice there was an increase in the numbers of total CD4(+) cells and activated (interleukin-2 receptor-expressing) CD4(+) cells in infected mice compared with the numbers in uninfected mice. Spleen cells from infected iNOS-deficient mice displayed increased proliferative responses and gamma interferon secretion when stimulated in vitro than those of control mice. These data suggest that NO production depresses T-helper 1-like responses generated during Trypanosoma brucei infections, thus promoting the survival of the parasite.

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KW - AFRICAN TRYPANOSOMIASIS

KW - SUPPRESSOR MACROPHAGES

KW - IN-VIVO

KW - IMMUNOSUPPRESSION

KW - INHIBITION

KW - INVITRO

KW - CATTLE

KW - CONGOLENSE

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SP - 3334

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JO - Infection and Immunity

JF - Infection and Immunity

SN - 0019-9567

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