Rosero Javier, Kima Peter E
Department of Microbiology and Cell Science, Gainesville, Florida, United States of America.
PLoS Pathog. 2025 Sep 16;21(9):e1013513. doi: 10.1371/journal.ppat.1013513. eCollection 2025 Sep.
Leishmania donovani (Ld) is the causative agent of visceral leishmaniasis, which results in death if not treated. In mammalian cells, Ld live in vacuolar compartments called Leishmania parasitophorous vacuoles (LdLPVs) that enigmatically divide following parasite replication. We evaluated the role of the endosomal sorting complex required for transport (ESCRT) machinery in the scission of LdLPVs. We found that ESCRT components are constitutively recruited to LdLPVs. We propose that this recruitment depends on the expression of PI(3,4)P2 on LdLPVs. The knockdown (KD) of upstream components of the ESCRT machinery revealed that ALIX, but not TSG101 or VPS28, led to a significant reduction in the parasite burden in infected cultures. Interestingly, LdLPVs in ALIXKDs were more distended and harbored more than 2 parasites. Incorporation of BrdU into Leishmania in THP-1 macrophages revealed that parasite replication was inhibited in ALIXKD due to defective LdLPV scission. These findings establish that non-canonical activation of the ESCRT machinery is required for Leishmania to replicate within macrophages.
杜氏利什曼原虫(Ld)是内脏利什曼病的病原体,如不治疗可导致死亡。在哺乳动物细胞中,Ld存在于称为利什曼原虫寄生泡(LdLPV)的液泡区室中,这些液泡在寄生虫复制后会神秘地分裂。我们评估了转运所需的内体分选复合物(ESCRT)机制在LdLPV分裂中的作用。我们发现ESCRT组分持续被招募到LdLPV。我们提出这种招募依赖于LdLPV上PI(3,4)P2的表达。ESCRT机制上游组分的敲低(KD)显示,ALIX而非TSG101或VPS28导致感染培养物中寄生虫负担显著降低。有趣的是,ALIX敲低细胞中的LdLPV更加膨胀,且含有不止2个寄生虫。将BrdU掺入THP-1巨噬细胞中的利什曼原虫表明,由于LdLPV分裂缺陷,ALIX敲低细胞中的寄生虫复制受到抑制。这些发现表明,利什曼原虫在巨噬细胞内复制需要ESCRT机制的非经典激活。