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()PH8和LV79菌株之间的表型差异可能会影响在哺乳动物宿主和白蛉中的生存。

Phenotypical Differences between () PH8 and LV79 Strains May Impact Survival in Mammal Host and in Phlebotomine Sand Flies.

作者信息

Tano Fabia Tomie, Telleria Erich Loza, Rêgo Felipe Dutra, Coelho Felipe Soares, de Rezende Eloiza, Soares Rodrigo Pedro, Traub-Cseko Yara Maria, Stolf Beatriz Simonsen

机构信息

Department of Parasitology, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-000, SP, Brazil.

Laboratório de Biologia Molecular de Parasitas e Vetores, Instituto Oswaldo Cruz, Fiocruz, Rio de Janeiro 21040-360, RJ, Brazil.

出版信息

Pathogens. 2023 Jan 22;12(2):173. doi: 10.3390/pathogens12020173.

DOI:10.3390/pathogens12020173
PMID:36839445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9965022/
Abstract

We previously showed that () promastigotes and amastigotes of the PH8 strain generated larger lesions in mice than LV79, and that lesion-derived amastigotes from the two strains differ in their proteomes. We recently reported that PH8 promastigotes are more phagocytized by macrophages. Promastigotes' membrane-enriched proteomes showed several differences, and samples of each strain clustered based on proteomes. In this paper, we show phenotypic differences between PH8 and LV79 promastigotes that may explain the higher virulence of PH8. We compared in vitro macrophage infections by day 4 (early) and day 6 (late stationary phase) cultures, resistance to complement, and LPG characteristics. PH8 promastigotes showed a higher infectivity and were more resistant to murine complement. LPG was different between the strains, which may influence the interaction with macrophages and survival to complement. We compared the infection of the permissive vector . PH8 was more abundant in the vector's gut 72 h after feeding, which is a moment where blood digestion is finished and the parasites are exposed to the gut environment. Our results indicate that PH8 promastigotes are more infective, more resistant to complement, and infect the permissive vector more efficiently. These data suggest that PH8 is probably better adapted to the sand fly and more prone to survive in the vertebrate host.

摘要

我们之前发现,PH8株的前鞭毛体和无鞭毛体在小鼠体内产生的损伤比LV79株更大,且来自这两个菌株的损伤源无鞭毛体的蛋白质组存在差异。我们最近报道,PH8前鞭毛体更容易被巨噬细胞吞噬。前鞭毛体富含膜的蛋白质组显示出一些差异,且每个菌株的样本根据蛋白质组聚类。在本文中,我们展示了PH8和LV79前鞭毛体之间的表型差异,这可能解释了PH8更高的毒力。我们比较了第4天(早期)和第6天(后期稳定期)培养物的体外巨噬细胞感染、对补体的抗性以及脂磷壁酸(LPG)特征。PH8前鞭毛体表现出更高的感染力,并且对鼠补体更具抗性。菌株之间的LPG不同,这可能影响与巨噬细胞的相互作用以及对补体的存活能力。我们比较了许可载体的感染情况。喂食后72小时,PH8在载体肠道中的含量更高,此时血液消化完成,寄生虫暴露于肠道环境中。我们的结果表明,PH8前鞭毛体更具感染力,对补体更具抗性,并且更有效地感染许可载体。这些数据表明,PH8可能更能适应白蛉,并且更易于在脊椎动物宿主中存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/29ca44bb09bb/pathogens-12-00173-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/13a1229b01a0/pathogens-12-00173-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/457307da41fa/pathogens-12-00173-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/bbc1e23f2915/pathogens-12-00173-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/50980cb43189/pathogens-12-00173-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/8d9ee0a6d34d/pathogens-12-00173-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/29ca44bb09bb/pathogens-12-00173-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/13a1229b01a0/pathogens-12-00173-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/457307da41fa/pathogens-12-00173-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/bbc1e23f2915/pathogens-12-00173-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/50980cb43189/pathogens-12-00173-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/8d9ee0a6d34d/pathogens-12-00173-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f2c/9965022/29ca44bb09bb/pathogens-12-00173-g006.jpg

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PLoS One. 2022 Aug 23;17(8):e0271492. doi: 10.1371/journal.pone.0271492. eCollection 2022.
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Major Molecular Factors Related to Pathogenicity.
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Mechanisms of Immunopathogenesis in Cutaneous Leishmaniasis And Post Kala-azar Dermal Leishmaniasis (PKDL).皮肤利什曼病和内脏利什曼病后皮肤利什曼病(PKDL)的免疫发病机制。
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