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首页> 外文期刊>Infection and immunity >FMS-Like Tyrosine Kinase 3 Ligand Treatment of Mice Aggravates Acute Lung Injury in Response to Streptococcus pneumoniae: Role of Pneumolysin
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FMS-Like Tyrosine Kinase 3 Ligand Treatment of Mice Aggravates Acute Lung Injury in Response to Streptococcus pneumoniae: Role of Pneumolysin

机译：FMS样酪氨酸激酶3配体治疗小鼠加重对肺炎链球菌的急性肺损伤：肺炎球菌溶血素的作用

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FMS-like tyrosine kinase-3 ligand (Flt3L) is a dendritic cell (DC) growth and differentiation factor with potential in antitumor therapies and antibacterial immunization strategies. However, the effect of systemic Flt3L treatment on lung-protective immunity against bacterial infection is incompletely defined. Here, we examined the impact of deficient (in Flt3L knockout [KO] mice), normal (in wild-type [WT] mice), or increased Flt3L availability (in WT mice pretreated with Flt3L for 3, 5, or 7 days) on lung DC subset profiles and lung-protective immunity against the major lung-tropic pathogen, Streptococcus pneumoniae. Although in Flt3L-deficient mice the numbers of DCs positive for CD11b (CD11bpos DCs) and for CD103 (CD103pos DCs) were diminished, lung permeability, a marker of injury, was unaltered in response to S. pneumoniae. In contrast, WT mice pretreated with Flt3L particularly responded with increased numbers of CD11bpos DCs and with less pronounced numbers of CD103pos DCs and impaired bacterial clearance and with increased lung permeability following S. pneumoniae challenge. Notably, infection of Flt3L-pretreated mice with S. pneumoniae lacking the pore-forming toxin, pneumolysin (PLY), resulted in substantially less lung CD11bpos DCs activation and reduced lung permeability. Collectively, this study establishes that Flt3L treatment enhances the accumulation of proinflammatory activated lung CD11bpos DCs which contribute to acute lung injury in response to PLY released by S. pneumoniae.
机译：FMS样酪氨酸激酶3配体（Flt3L）是树突状细胞（DC）的生长和分化因子，在抗肿瘤治疗和抗菌免疫策略中具有潜力。但是，全身性Flt3L治疗对针对细菌感染的肺保护免疫的作用尚未完全确定。在这里，我们检查了缺陷小鼠（在Flt3L基因敲除[KO]小鼠中），正常动物（在野生型[WT]小鼠中）或Flt3L可用性增加（在用Flt3L预处理3、5或7天的WT小鼠中）的影响肺DC子集谱和针对主要的热带肺病病原体肺炎链球菌的肺保护免疫。尽管在缺乏Flt3L的小鼠中，CD11b（CD11bpos DCs）和CD103（CD103pos DCs）阳性DC的数量减少了，但是肺损伤通透性（肺损伤链球菌）并未改变。相反，用Flt3L预处理的WT小鼠在肺炎链球菌感染后，CD11bpos DC的数量增加，CD103pos DC的数量减少，细菌清除率降低，肺通透性增加。值得注意的是，用Flt3L预处理的小鼠感染的肺炎链球菌缺乏致孔毒素，即肺炎球菌溶血素（PLY），导致肺CD11bpos DC的激活大大减少，肺通透性降低。总体而言，该研究确定Flt3L治疗可增强促炎性激活的肺CD11bpos DC的积累，这对由肺炎链球菌释放的PLY引起的急性肺损伤有贡献。

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