Department of Cell Biology, School of Medicine of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
mBio. 2024 Nov 13;15(11):e0198023. doi: 10.1128/mbio.01980-23. Epub 2024 Oct 11.
Parasites from the genus are the causative agents of leishmaniasis and primarily reside within macrophages during mammalian infection. Their ability to establish intracellular infection provides a secure niche for proliferation while evading detection. However, successful multiplication within mammalian cells requires the orchestration of multiple mechanisms that control host cell viability. In contrast, innate immune cells, such as macrophages, can undergo different forms of cell death in response to pathogenic intracellular microbes. Thus, modulation of these different forms of host cell death is crucial for Leishmaniasis development. The regulation of host cell apoptosis, a form of programmed cell death, is crucial for sustaining parasites within viable host cells. Accordingly, several studies have demonstrated evasion of apoptosis induced by dermotropic and viscerotropic species. Conversely, the prevention of pyroptosis, an inflammatory form of cell death, ensures the establishment of infection by silencing the release of mediators that could trigger massive proinflammatory responses. This manuscript explores how regulates various host cell death pathways and overviews seminal studies on regulating host cell apoptosis by different species.
属寄生虫是利什曼原虫病的病原体,主要在哺乳动物感染期间存在于巨噬细胞内。它们能够建立细胞内感染,为增殖提供了一个安全的小生境,同时逃避检测。然而,要在哺乳动物细胞内成功繁殖,需要协调多种机制来控制宿主细胞的活力。相比之下,先天免疫细胞,如巨噬细胞,在受到致病性细胞内微生物的刺激时,会经历不同形式的细胞死亡。因此,宿主细胞死亡的这些不同形式的调节对于利什曼原虫病的发展至关重要。宿主细胞凋亡的调节,即程序性细胞死亡的一种形式,对于维持寄生虫在有活力的宿主细胞内的存活至关重要。因此,有几项研究表明,皮肤亲和性和内脏亲和性物种逃避了凋亡诱导。相反,通过沉默可能引发大规模促炎反应的介质的释放来防止细胞焦亡(一种炎症形式的细胞死亡),可确保感染的建立。本文探讨了属寄生虫如何调节各种宿主细胞死亡途径,并概述了不同属寄生虫调节宿主细胞凋亡的重要研究。