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几丁质酶样蛋白 TgCLP1 调节寄生虫包囊负荷。

chitinase-like protein TgCLP1 regulates the parasite cyst burden.

机构信息

Laboratory of Sustainable Animal Environment, Graduate School of Agricultural Science, Tohoku University, Osaki, Miyagi, Japan.

Department of Parasitology, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.

出版信息

Front Cell Infect Microbiol. 2024 May 17;14:1359888. doi: 10.3389/fcimb.2024.1359888. eCollection 2024.

Abstract

, an important intracellular parasite of humans and animals, causes life-threatening toxoplasmosis in immunocompromised individuals. Although secretory proteins during acute infection (tachyzoite, which divides rapidly and causes inflammation) have been extensively characterized, those involved in chronic infection (bradyzoite, which divides slowly and is surrounded by a cyst wall) remain uncertain. Regulation of the cyst wall is essential to the parasite life cycle, and polysaccharides, such as chitin, in the cyst wall are necessary to sustain latent infection. secretory proteins during the bradyzoite stage may have important roles in regulating the cyst wall via polysaccharides. Here, we focused on characterizing the hypothetical chitinase, chitinase-like protein 1 (TgCLP1). We found that the chitinase-like domain containing TgCLP1 is partially present in the bradyzoite microneme and confirmed, albeit partially, its previous identification in the tachyzoite microneme. Furthermore, although parasites lacking TgCLP1 could convert from tachyzoites to bradyzoites and make an intact cyst wall, they failed to convert from bradyzoites to tachyzoites, indicating that TgCLP1 is necessary for bradyzoite reactivation. Taken together, our findings deepen our understanding of the molecular basis of recrudescence and could contribute to the development of novel strategies for the control of toxoplasmosis.

摘要

弓形虫是一种重要的人类和动物细胞内寄生虫,可导致免疫功能低下个体发生危及生命的弓形体病。虽然急性感染(快速分裂并引起炎症的速殖子)期间的分泌蛋白已得到广泛研究,但慢性感染(缓慢分裂并被囊壁包围的缓殖子)期间的分泌蛋白仍不确定。囊壁的调节对于寄生虫的生命周期至关重要,囊壁中的多糖(如几丁质)对于维持潜伏感染是必需的。缓殖子阶段的分泌蛋白可能通过多糖在调节囊壁方面发挥重要作用。在这里,我们专注于表征假定的几丁质酶、几丁质酶样蛋白 1(TgCLP1)。我们发现 TgCLP1 含有几丁质酶样结构域,部分存在于缓殖子微线体中,并证实了其在速殖子微线体中的先前鉴定。此外,尽管缺乏 TgCLP1 的寄生虫能够从速殖子转化为缓殖子并形成完整的囊壁,但它们不能从缓殖子转化为速殖子,这表明 TgCLP1 对于缓殖子的再激活是必需的。总之,我们的研究结果加深了对复发分子基础的理解,并可能有助于开发新的弓形虫病控制策略。

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