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Binding of Leishmania infantum Lipophosphoglycan to the Midgut Is Not Sufficient To Define Vector Competence in Lutzomyia longipalpis Sand Flies.
mSphere ( IF 4.8 ) Pub Date : 2020-09-09 , DOI: 10.1128/msphere.00594-20
Iliano V Coutinho-Abreu 1 , James Oristian 2 , Waldionê de Castro 2 , Timothy R Wilson 2 , Claudio Meneses 2 , Rodrigo P Soares 3 , Valéria M Borges 4 , Albert Descoteaux 5 , Shaden Kamhawi 1 , Jesus G Valenzuela 1
Affiliation  

The major surface lipophosphoglycan (LPG) of Leishmania parasites is critical to vector competence in restrictive sand fly vectors in mediating Leishmania attachment to the midgut epithelium, considered essential to parasite survival and development. However, the relevance of LPG for sand flies that harbor multiple species of Leishmania remains elusive. We tested binding of Leishmania infantum wild-type (WT), LPG-defective (Δlpg1 mutants), and add-back (Δlpg1 + LPG1) lines to sand fly midguts in vitro and their survival in Lutzomyia longipalpis sand flies in vivo. Le. infantum WT parasites attached to the Lu. longipalpis midgut in vitro, with late-stage parasites binding to midguts in significantly higher numbers than were seen with early-stage promastigotes. Δlpg1 mutants did not bind to Lu. longipalpis midguts, and this was rescued in the Δlpg1 + LPG1 lines, indicating that midgut binding is mediated by LPG. When Lu. longipalpis sand flies were infected with the Le. infantum WT or Le. infantum Δlpg1 or Le. infantum Δlpg1 + LPG1 line of the BH46 or BA262 strains, the BH46 Δlpg1 mutant, but not the BA262 Δlpg1 mutant, survived and grew to numbers similar to those seen with the WT and Δlpg1 + LPG1 lines. Exposure of BH46 and BA262 Δlpg1 mutants to blood-engorged midgut extracts led to mortality of the BA262 Δlpg1 but not the BH46 Δlpg1 parasites. These findings suggest that Le. infantum LPG protects parasites on a strain-specific basis early in infection, likely against toxic components of blood digestion, but that it is not necessary to prevent Le. infantum evacuation along with the feces in the permissive vector Lu. longipalpis.

中文翻译:

婴儿利什曼原虫脂磷聚糖与中肠的结合不足以在 Lutzomyia longipalpis 沙蝇中定义载体能力。

利什曼原虫寄生虫的主要表面脂磷聚糖 (LPG) 对限制性白蛉载体在介导利什曼原虫与中肠上皮的附着方面的能力至关重要,被认为对寄生虫的生存和发育至关重要。然而,液化石油气与携带多种利什曼原虫的沙蝇的相关性仍然难以捉摸。我们测试了结合婴儿利什曼原虫(WT),LPG缺陷(Δ的野生型LPG1突变体),并添加回(Δ LPG1 + LPG1)线白蛉肠体外和它们在生存Lutzomyia长须罗蛉白蛉体内乐。infantum WT 寄生虫附着于鲁。longipalpis中肠体外,晚期寄生虫与中肠结合的数量明显高于早期前鞭毛体。Δ lpg1突变体不与Lu结合longipalpis 中肠,这在 Δ lpg1 + LPG1系中被拯救,表明中肠结合是由 LPG 介导的。当卢。longipalpis沙蝇被勒感染婴儿WT 或Le。婴儿Δ lpg1Le。婴儿Δ lpg1 + LPG1在 BH46 或 BA262 菌株系中,BH46 Δ lpg1突变体,但不是 BA262 Δ lpg1突变体,存活并生长到与 WT 和 Δ lpg1 + LPG1系所见相似的数量。BH46 和 BA262 Δ lpg1突变体暴露于充血的中肠提取物会导致 BA262 Δ lpg1而非 BH46 Δ lpg1寄生虫的死亡。这些发现表明Le. 婴儿LPG 在感染早期以菌株特异性为基础保护寄生虫,可能对抗血液消化的有毒成分,但没有必要预防Le。婴儿随粪便排出体外鲁。长须罗蛉
更新日期:2020-09-10
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