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非荚膜型肺炎链球菌毒力的液体琼脂肺炎模型研究。

Investigation on the virulence of non-encapsulated Streptococcus pneumoniae using liquid agar pneumonia model.

机构信息

Department of Otorhinolaryngology-Head and Neck Surgery, Wakayama Medical University, Kimiidera 811-1, Wakayama City, Wakayama, 641-8509, Japan.

Department of Otorhinolaryngology-Head and Neck Surgery, Wakayama Medical University, Kimiidera 811-1, Wakayama City, Wakayama, 641-8509, Japan; Sugita ENT Clinic, Mihama-Ku Takasu 3-14-1, Chiba City, Chiba, 261-0004, Japan.

出版信息

J Infect Chemother. 2022 Nov;28(11):1452-1458. doi: 10.1016/j.jiac.2022.07.003. Epub 2022 Jul 11.

DOI:10.1016/j.jiac.2022.07.003
PMID:35835387
Abstract

INTRODUCTION

Since the introduction of pneumococcal conjugate vaccine, there have been warnings of an increase in infections caused by non-vaccine type of Streptococcus pneumoniae strains. Among them, nonencapsulated Streptococcus pneumoniae (NESp) has been reported to cause invasive infections, especially in children and the elderly. Due to low virulence, however, basic experimental reports on invasive infections are limited.

METHODS

We applied a liquid-agar method to establish a mouse model of invasive NESp infection. Mice were intratracheally administered a bacterial suspension including agar. With this technique, we investigated the pathogenicity of NESp and the effect of Pneumococcal surface protein K (PspK), a specific surface protein antigen of NESp. NESp wild-type strain (MNZ11) and NESp pspK-deleted mutant strain (MNZ1131) were used in this study. The survival rate, number of bacteria, cytokine/chemokine levels in the bronchoalveolar lavage fluid, and histology of the lung tissue were evaluated.

RESULTS

Mice that were intratracheally administered MNZ11 developed lethal pneumonia with bacteremia within 48 h. Conversely, MNZ1131 showed predominantly low lethality without significant pro-inflammatory cytokine production. NESp was found to cause severe pneumonia and bacteremia upon reaching the lower respiratory tract, and PspK was a critical factor of NESp for developing invasive infections.

CONCLUSIONS

The current study demonstrated the ability of NESp to develop invasive diseases, especially in connection with PspK by use of a mouse pneumonia model.

摘要

简介

自肺炎球菌结合疫苗问世以来,人们一直担心非疫苗型肺炎链球菌菌株引起的感染会增加。其中,无荚膜肺炎链球菌(NESp)已被报道可引起侵袭性感染,尤其是在儿童和老年人中。然而,由于其毒力较低,侵袭性感染的基础实验报道有限。

方法

我们应用液体琼脂法建立了一种侵袭性 NESp 感染的小鼠模型。通过气管内给予含琼脂的细菌悬浮液来进行实验。利用这项技术,我们研究了 NESp 的致病性以及 NESp 表面蛋白 K(PspK)的作用,PspK 是 NESp 的一种特定表面蛋白抗原。本研究使用了 NESp 野生型菌株(MNZ11)和 NESp pspK 缺失突变株(MNZ1131)。评估了小鼠的存活率、肺泡灌洗液中的细菌数量、细胞因子/趋化因子水平以及肺组织的组织学变化。

结果

气管内给予 MNZ11 的小鼠在 48 小时内发展为致死性肺炎合并菌血症。相反,MNZ1131 主要表现为低致死率,且无明显促炎细胞因子产生。NESp 进入下呼吸道后可引起严重的肺炎和菌血症,而 PspK 是 NESp 引发侵袭性感染的关键因素。

结论

本研究通过小鼠肺炎模型,证明了 NESp 特别是与 PspK 相关的侵袭性疾病的能力。

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