Abstract

Background

Otitis media (OM) is a common and potentially serious disease of childhood. Although OM is multifactorial on origin, bacterial infection is a unifying component. Many studies have established a critical role for innate immunity in bacterial clearance and OM resolution. A key component of innate immunity is the recruitment of immune and inflammatory cells, including macrophages.

Methods

To explore the role of macrophages in OM, we evaluated the expression of genes related to macrophage function during a complete episode of acute OM in the mouse caused by middle ear (ME) inoculation with Haemophilus influenzae. We also combined CCR2 deficiency with chlodronate liposome toxicity to deplete macrophages during OM.

Results

Macrophage genes were robustly regulated during OM. Moreover, macrophage depletion enhanced and prolonged the infiltration of neutrophils into the infected ME and increased the persistence of bacterial infection.

Conclusions

The results illustrate the critical role played by macrophages in OM resolution.

中文翻译：

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CCR2-/- 小鼠巨噬细胞耗竭延迟细菌清除并增强急性中耳炎模型中的中性粒细胞浸润

摘要

背景

中耳炎 (OM) 是一种常见且可能严重的儿童疾病。尽管 OM 的起源是多因素的，但细菌感染是一个统一的组成部分。许多研究已经确立了先天免疫在细菌清除和 OM 解决中的关键作用。先天免疫的一个关键组成部分是免疫和炎症细胞的募集，包括巨噬细胞。

方法

为了探索巨噬细胞在 OM 中的作用，我们评估了在由中耳 (ME) 接种流感嗜血杆菌引起的小鼠急性 OM 完整发作期间与巨噬细胞功能相关的基因表达。我们还将 CCR2 缺陷与氯膦酸盐脂质体毒性相结合，以在 OM 期间消耗巨噬细胞。

结果

巨噬细胞基因在 OM 期间受到强烈调控。此外，巨噬细胞耗竭增强并延长了中性粒细胞向受感染 ME 的浸润，并增加了细菌感染的持续性。

结论

结果说明了巨噬细胞在 OM 分辨率中所起的关键作用。