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首页> 外文期刊>Infection and immunity >Sensing of Interleukin-1 Cytokines during Streptococcus pneumoniae Colonization Contributes to Macrophage Recruitment and Bacterial Clearance
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Sensing of Interleukin-1 Cytokines during Streptococcus pneumoniae Colonization Contributes to Macrophage Recruitment and Bacterial Clearance

机译：肺炎链球菌定植过程中白介素1细胞因子的感觉有助于巨噬细胞招募和细菌清除。

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Streptococcus pneumoniae (the pneumococcus), a leading cause of bacterial disease, is most commonly carried in the human nasopharynx. Colonization induces inflammation that promotes the organism's growth and transmission. This inflammatory response is dependent on intracellular sensing of bacterial components that access the cytosolic compartment via the pneumococcal pore-forming toxin pneumolysin. In vitro, cytosolic access results in cell death that includes release of the proinflammatory cytokine interleukin-1β (IL-1β). IL-1 family cytokines, including IL-1β, are secreted upon activation of inflammasomes, although the role of this activation in the host immune response to pneumococcal carriage is unknown. Using a murine model of pneumococcal nasopharyngeal colonization, we show that mice deficient in the interleukin-1 receptor type 1 (Il1r1?/?) have reduced numbers of neutrophils early after infection, fewer macrophages later in carriage, and prolonged bacterial colonization. Moreover, intranasal administration of Il-1β promoted clearance. Macrophages are the effectors of clearance, and characterization of macrophage chemokines in colonized mice revealed that Il1r1?/? mice have lower expression of the C-C motif chemokine ligand 6 (CCL6), correlating with reduced macrophage recruitment to the nasopharynx. IL-1 family cytokines are known to promote adaptive immunity; however, we observed no difference in the development of humoral or cellular immunity to pneumococcal colonization between wild-type and Il1r1?/? mice. Our findings show that sensing of IL-1 cytokines during colonization promotes inflammation without immunity, which may ultimately benefit the pneumococcus.
机译：肺炎链球菌（肺炎球菌）是细菌性疾病的主要原因，最常见于人类鼻咽。定植引起炎症，促进生物的生长和传播。这种炎症反应取决于通过肺炎球菌成孔毒素肺炎球菌溶血素进入胞质区室的细菌成分的细胞内感测。 在体外，胞质进入导致细胞死亡，其中包括促炎性细胞因子白介素1β（IL-1β）的释放。 IL-1家族的细胞因子，包括IL-1β，是在炎性体激活时分泌的，尽管这种激活在宿主对肺炎球菌携带的免疫反应中的作用尚不清楚。使用鼠肺炎球菌鼻咽部定植的小鼠模型，我们发现感染白细胞介素1受体1（ Il1r1 ？/？）1型缺陷的小鼠感染后中性粒细胞数量减少，较少的巨噬细胞随后运输以及细菌定殖时间延长。此外，鼻内给药II-1β可促进清除。巨噬细胞是清除的效应物，定居小鼠中巨噬细胞趋化因子的特征表明 Il1r1 ？/？小鼠的CC基序趋化因子配体6（CCL6）表达较低，与减少巨噬细胞向鼻咽募集相关。已知IL-1家族细胞因子可促进适应性免疫。但是，我们观察到野生型和 Il1r1 ？/？小鼠的针对肺炎球菌定植的体液免疫或细胞免疫发育没有差异。我们的发现表明，在定居过程中感测IL-1细胞因子可促进炎症而无免疫力，这可能最终使肺炎球菌受益。

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