嗜碱性粒细胞耗竭改变宿主免疫、肠道通透性和哺乳动物疟疾宿主-蚊子传播。

Erinn L Donnelly, Nora Céspedes, Gretchen Hansten, Delaney Wagers, Anna M Briggs, Casey Lowder, Joseph Schauer, Sarah M Garrison, Lori Haapanen, Judy Van de Water, Shirley Luckhart
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引用次数: 4

摘要

疟疾引起的菌血症已被证明是由肠肥大细胞(MC)激活引起的。回肠MCs的出现和肠道对肠道细菌通透性的增加是由早期th2偏向性宿主对感染的免疫反应引起的,其特征是IL-4、IL-10、肥大细胞蛋白酶(Mcpt)1和Mcpt4的出现,以及循环中嗜碱性粒细胞和嗜酸性粒细胞的增加。鉴于嗜碱性粒细胞和MCs在过敏性炎症中的功能相似性,以及嗜碱性粒细胞产生大量IL-4的能力,我们试图确定嗜碱性粒细胞在增加肠道通透性、MCs流入和疟疾背景下菌血症发展中的作用。在感染非致死性约氏疟原虫约氏17XNL后,缺乏嗜碱性粒细胞的Basoph8 × ROSA-DTα小鼠或baso(-)小鼠表现出肠道通透性增加和回肠MC数量增加,而血液中细菌16S核糖体DNA拷贝数没有增加。对回肠细胞因子、趋化因子和mc相关因子的分析显示,与baso(+)小鼠相比,baso(-)小鼠感染后第6天TNF-α和IL-13显著升高。此外,对相关宿主免疫因子的网络分析显示,baso(-)和baso(+)小鼠感染后对寄生虫和易位细菌的全身和回肠反应存在深刻差异。最后,嗜碱性粒细胞的减少与配子体和寄生虫向按蚊传播的显著增加有关,这表明嗜碱性粒细胞在控制配子体和反过来控制哺乳动物宿主到蚊子的寄生虫传播方面发挥了先前未被描述的作用。
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Basophil Depletion Alters Host Immunity, Intestinal Permeability, and Mammalian Host-to-Mosquito Transmission in Malaria.

Malaria-induced bacteremia has been shown to result from intestinal mast cell (MC) activation. The appearance of MCs in the ileum and increased intestinal permeability to enteric bacteria are preceded by an early Th2-biased host immune response to infection, characterized by the appearance of IL-4, IL-10, mast cell protease (Mcpt)1 and Mcpt4, and increased circulating basophils and eosinophils. Given the functional similarities of basophils and MCs in the context of allergic inflammation and the capacity of basophils to produce large amounts of IL-4, we sought to define the role of basophils in increased intestinal permeability, in MC influx, and in the development of bacteremia in the context of malaria. Upon infection with nonlethal Plasmodium yoelii yoelii 17XNL, Basoph8 × ROSA-DTα mice or baso (-) mice that lack basophils exhibited increased intestinal permeability and increased ileal MC numbers, without any increase in bacterial 16S ribosomal DNA copy numbers in the blood, relative to baso (+) mice. Analysis of cytokines, chemokines, and MC-associated factors in the ileum revealed significantly increased TNF-α and IL-13 at day 6 postinfection in baso (-) mice compared with baso (+) mice. Moreover, network analysis of significantly correlated host immune factors revealed profound differences between baso (-) and baso (+) mice following infection in both systemic and ileal responses to parasites and translocated bacteria. Finally, basophil depletion was associated with significantly increased gametocytemia and parasite transmission to Anopheles mosquitoes, suggesting that basophils play a previously undescribed role in controlling gametocytemia and, in turn, mammalian host-to-mosquito parasite transmission.

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