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肺炎链球菌与人咽细胞相互作用的表型、基因组和转录组特征。

Phenotypic, genomic, and transcriptional characterization of Streptococcus pneumoniae interacting with human pharyngeal cells.

机构信息

Kenya Medical Research Institute, Wellcome Trust Research Programme, Kilifi, Kenya.

出版信息

BMC Genomics. 2013 Jun 9;14:383. doi: 10.1186/1471-2164-14-383.

DOI:10.1186/1471-2164-14-383
PMID:23758733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3708772/
Abstract

BACKGROUND

Streptococcus pneumoniae is a leading cause of childhood morbidity and mortality worldwide, despite the availability of effective pneumococcal vaccines. Understanding the molecular interactions between the bacterium and the host will contribute to the control and prevention of pneumococcal disease.

RESULTS

We used a combination of adherence assays, mutagenesis and functional genomics to identify novel factors involved in adherence. By contrasting these processes in two pneumococcal strains, TIGR4 and G54, we showed that adherence and invasion capacities vary markedly by strain. Electron microscopy showed more adherent bacteria in association with membranous pseudopodia in the TIGR4 strain. Operons for cell wall phosphorylcholine incorporation (lic), manganese transport (psa) and phosphate utilization (phn) were up-regulated in both strains on exposure to epithelial cells. Pneumolysin, pili, stress protection genes (adhC-czcD) and genes of the type II fatty acid synthesis pathway were highly expressed in the naturally more invasive strain, TIGR4. Deletion mutagenesis of five gene regions identified as regulated in this study revealed attenuation in adherence. Most strikingly, ∆SP_1922 which was predicted to contain a B-cell epitope and revealed significant attenuation in adherence, appeared to be expressed as a part of an operon that includes the gene encoding the cytoplasmic pore-forming toxin and vaccine candidate, pneumolysin.

CONCLUSION

This work identifies a list of novel potential pneumococcal adherence determinants.

摘要

背景

尽管有有效的肺炎球菌疫苗，但肺炎球菌仍是导致全球儿童发病和死亡的主要原因。了解细菌和宿主之间的分子相互作用将有助于控制和预防肺炎球菌病。

结果

我们使用了结合黏附测定、突变和功能基因组学的方法来鉴定参与黏附的新的因子。通过对比两种肺炎球菌菌株 TIGR4 和 G54 的这些过程，我们表明菌株之间的黏附能力和侵袭能力差异很大。电子显微镜显示，在 TIGR4 菌株中，与膜状伪足相关的细菌更具黏附性。在暴露于上皮细胞时，细胞壁磷酸胆碱掺入（lic）、锰转运（psa）和磷酸盐利用（phn）操纵子在两种菌株中均上调。肺炎球菌溶血素、菌毛、应激保护基因（adhC-czcD）和 II 型脂肪酸合成途径的基因在自然侵袭性更强的菌株 TIGR4 中高度表达。对本研究中发现的五个受调控的基因区域进行缺失突变显示黏附能力减弱。最引人注目的是，ΔSP_1922 被预测包含 B 细胞表位，并且黏附能力明显减弱，似乎作为包含编码细胞质孔形成毒素和疫苗候选物肺炎球菌溶血素的基因的操纵子的一部分表达。

结论

这项工作确定了一系列新的潜在肺炎球菌黏附决定因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/695e/3708772/19775e8410d1/1471-2164-14-383-7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/695e/3708772/19775e8410d1/1471-2164-14-383-7.jpg
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