Cytokine Production Assayed by RT-PCR in Pregnant Mice Infected by Toxoplasma gondii as a Model of Congenital Toxoplasmosis.

  • HE NA
    Department of Medical Zoology, Nagasaki University School of Medicine Department of Parasitology, Chiba University School of Medicine
  • AOSAI FUMIE
    Department of Parasitology, Chiba University School of Medicine
  • HYE-SEONG MUN
    Department of Parasitology, Chiba University School of Medicine
  • SEKIYA SOUEI
    Department of Obstetrics and Gynecology, Chiba University School of Medicine
  • YANO AKIHIKO
    Department of Parasitology, Chiba University School of Medicine

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  • Cytokine Production Assayed by RT-PCR i

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To explore the mechanisms of immune responses of host to Toxoplasma gondii (T. gondii) infection in pregnant mice, we evaluated roles of cytokines [interferon gamma (IFN-γ), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and interleukin 4 (IL-4)] by measuring mRNAs of these cytokines in placentas, lungs and spleens. The pathogenic effects of time and duration of the Fukaya infection on cytokine mRNA levels in pregnant mice were analyzed. The abundance of mRNAs encoding these cytokines was measured by reverse transcriptase (RT) -PCR at early and late stages of pregnancy in various organs of both susceptible C57BL/6 and resistant BALB/c pregnant mice infected with T. gondii. IFN-γ and TNF-α but not IL-6 or IL-4, were predominant in the immune responses of placentas, lungs and spleens of BALB/c and C57BL/6 mice during T. gondii infection. Levels of IFN-γ and TNF-α mRNA in placentas of early stage pregnant BALB/c mice (infected at one-week pregnancy and examined on day 4 after infection; 1W4D) were higher than those in corresponding C57BL/6 pregnant mice, which might correlate with the fact that higher parasite numbers in placentas and lungs of C57BL/6 mice (infected at one-week pregnancy and examined on day 11 after the Fukaya infection; 1W11D) were observed than those in placentas and lungs of corresponding BALB/c mice, but not correlate with the result of parasite numbers (T. gondii No./mg tissue) in spleens of C57BL/6 (0) and BALB/c (120±56) pregnant mice. In the late stage of pregnancy, levels of IFN-γ and TNF-a did not show definite correlations with T. gondii loads in placentas, lungs and spleens. These results indicate that endogenous IFN-γ and TNF-a of early stage pregnancy may be essential for inhibition of T. gondii growth in some organs (placentas and lungs), but not in spleens, and the mechanisms of genetic influence involved in the susceptibility and resistance to acute T. gondii infection may include several immune responses acting together.

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