Chowdhury Debabrata, Sharma Manu, Jahng James W S, Singh Upinder
Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California 94305, USA.
Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California 94305, USA.
J Parasitol Res. 2024 Oct 29;2024:7325606. doi: 10.1155/2024/7325606. eCollection 2024.
Recent studies have shown that extracellular vesicles (EVs) secreted by various parasites are capable of modulating the host's innate immune responses, such as by altering macrophage (M) phenotypes and functions. Studies have shown that M promote early host responses to amoebic infection by releasing proinflammatory cytokines that are crucial to combating amoebiasis. Here, we are reporting for the first time the effect of EVs released by (EVs) on human THP-1 differentiated M (THP-1 M). We show that the EVs are internalized by THP-1 M which leads to differential regulation of various cytokines associated with both M1 and M2 M. We also saw that EV treatment thwarted Type 2 immune-response-related transcriptome pSTAT6 in the THP-1 M. Furthermore, EVs stimulated M to reduce their energy demand by suppressing oxidative phosphorylation (OXPHOS) and adenosine triphosphate (ATP) production. Hence, the human parasite -derived EVs are capable of eliciting an immune response from M that may contribute to overall infection status.
最近的研究表明，各种寄生虫分泌的细胞外囊泡（EVs）能够调节宿主的固有免疫反应，例如通过改变巨噬细胞（M）的表型和功能。研究表明，M通过释放对对抗阿米巴病至关重要的促炎细胞因子来促进宿主对阿米巴感染的早期反应。在这里，我们首次报道了 （EVs）释放的EVs对人THP-1分化的M（THP-1 M）的影响。我们表明，EVs被THP-1 M内化，这导致与M1和M2 M相关的各种细胞因子的差异调节。我们还发现，EV处理阻碍了THP-1 M中与2型免疫反应相关的转录组pSTAT6。此外，EVs刺激M通过抑制氧化磷酸化（OXPHOS）和三磷酸腺苷（ATP）的产生来降低其能量需求。因此，源自人类寄生虫的EVs能够引发M的免疫反应，这可能有助于整体感染状态。
