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铜绿假单胞菌和缓症链球菌混合感染对急性肺炎小鼠模型中TLR4介导的免疫反应的影响

Effects of Pseudomonas aeruginosa and Streptococcus mitis mixed infection on TLR4-mediated immune response in acute pneumonia mouse model.

作者信息

Song Chao, Li Hongdong, Zhang Yunhui, Yu Jialin

机构信息

Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China.

Ministry of Education Key Laboratory of Child Development and Disorders - Chongqing Key Laboratory of Pediatrics, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing, China.

出版信息

BMC Microbiol. 2017 Apr 4;17(1):82. doi: 10.1186/s12866-017-0999-1.

Abstract

BACKGROUND

Our previous research on the diversity of microbiota in the endotracheal tubes (ETTs) of neonates in the neonatal intensive care unit found that Pseudomonas aeruginosa (P. aeruginosa) and Streptococcus mitis (S. mitis) were the dominant bacteria on the ETT surface and the existence of S. mitis could promote biofilm formation and pathogenicity of P. aeruginosa. Toll-like receptor 4 (TLR4), which has been widely detected on the surface of airway epithelial cells, is the important component of the innate immune system. Therefore, we hypothesized that the co-existence of these two bacteria might impact the host immune system through TLR4 signaling.

RESULTS

S. mitis rarely caused inflammation, whereas P. aeruginosa caused the most severe inflammation accompanied by increases in the number of inflammatory cells, interleukin (IL)-6 and tumor necrosis factor (TNF)-α expression, and total cell counts in BALF (p < 0.05). In the PAO1 + S. mitis group, moderate inflammation, reduced IL-6 and TNF-α protein levels, and decreased total cell counts were observed. Additionally, levels of these indicators were decreased lower in TLR4-deficient mice than in wild-type mice (p < 0.05).

CONCLUSIONS

Our results demonstrated that infection with S. mitis together with P. aeruginosa could alleviate lung inflammation in acute lung infection mouse models possibly via the TLR4 signaling pathway.

摘要

背景

我们之前对新生儿重症监护病房新生儿气管内插管(ETT)中微生物群多样性的研究发现,铜绿假单胞菌(P. aeruginosa)和缓症链球菌(S. mitis)是ETT表面的主要细菌,且缓症链球菌的存在可促进铜绿假单胞菌生物膜的形成和致病性。Toll样受体4(TLR4)在气道上皮细胞表面广泛表达,是固有免疫系统的重要组成部分。因此,我们推测这两种细菌的共存可能通过TLR4信号通路影响宿主免疫系统。

结果

缓症链球菌很少引起炎症,而铜绿假单胞菌引起最严重的炎症,伴有炎性细胞数量增加、白细胞介素(IL)-6和肿瘤坏死因子(TNF)-α表达增加以及支气管肺泡灌洗液(BALF)中总细胞计数增加(p < 0.05)。在PAO1 + 缓症链球菌组中,观察到中度炎症、IL-6和TNF-α蛋白水平降低以及总细胞计数减少。此外,这些指标在TLR4缺陷小鼠中的降低程度低于野生型小鼠(p < 0.05)。

结论

我们的结果表明,在急性肺部感染小鼠模型中,缓症链球菌与铜绿假单胞菌共同感染可能通过TLR4信号通路减轻肺部炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/bdef4b8300f6/12866_2017_999_Fig1_HTML.jpg

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