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缺乏干扰素-γ诱导基因IGTP并不会显著改变感染克氏锥虫(巴西株)的小鼠恰加斯心肌病的发展。

Absence of interferon-gamma-inducible gene IGTP does not significantly alter the development of chagasic cardiomyopathy in mice infected with Trypanosoma cruzi (Brazil strain).

作者信息

de Souza A P, Tang B, Tanowitz H B, Factor S M, Shtutin V, Shirani J, Taylor G A, Weiss L M, Jelicks L A

机构信息

Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

出版信息

J Parasitol. 2003 Dec;89(6):1237-9. doi: 10.1645/GE-3185RN.

Abstract

Interferon-gamma (IFN-gamma) contributes to host resistance during acute infection with Trypanosoma cruzi, the causative agent of Chagas' disease. Inducibly expressed guanosine triphosphatase (IGTP), a 48-kDa guanosine triphosphatase (GTPase), is a member of a family of GTPase proteins inducibly expressed by IFN-gamma. The expression pattern of IGTP suggests that it may mediate IFN-gamma-induced responses in a variety of cell types. IGTP has been demonstrated to be important for control of Toxoplasma gondii infection but not for resistance against Listeria monocytogenes. We evaluated the role of IGTP in development of chronic chagasic cardiomyopathy in IGTP null mice and C57X129sv (wild type [WT]) mice infected with the Brazil strain for 6 mo. There was no significant difference in parasitemia or cardiac histopathology between null and WT mice. Right ventricular remodeling was observed in infected IGTP null mice, suggesting that IGTP does not significantly alter the course of T. cruzi infection.

摘要

γ干扰素(IFN-γ)在恰加斯病病原体克氏锥虫急性感染期间有助于宿主抵抗。可诱导表达的鸟苷三磷酸酶(IGTP)是一种48 kDa的鸟苷三磷酸酶(GTP酶),是由IFN-γ诱导表达的GTP酶蛋白家族的成员。IGTP的表达模式表明它可能介导IFN-γ在多种细胞类型中诱导的反应。IGTP已被证明对控制弓形虫感染很重要,但对抵抗单核细胞增生李斯特菌不重要。我们评估了IGTP基因敲除小鼠和感染巴西株6个月的C57X129sv(野生型[WT])小鼠中IGTP在慢性恰加斯病性心肌病发展中的作用。基因敲除小鼠和野生型小鼠之间的寄生虫血症或心脏组织病理学没有显著差异。在感染的IGTP基因敲除小鼠中观察到右心室重塑,这表明IGTP不会显著改变克氏锥虫感染的进程。

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