Transcriptional adaptation of pneumococci and human pharyngeal cells in the presence of a virus infection

BMC Genomics

Research Article

Nikhil Kumar¹  Nadeeza Ishmael¹  Valerie Grinblat-Huse¹  David R Riley¹  Hervé Tettelin¹  Julie C Dunning Hotopp¹  George M Carlone²  Sandra Romero-Steiner²  Jacquelyn Sampson²  Teresa C T Peret³  Dean D Erdman³  Sheila Z Kimaro Mlacha⁴  J Anthony G Scott⁵ 

[1] Department of Microbiology and Immunology, Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, USA;Division of Bacterial Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA;Division of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA;Kenya Medical Research Institute, Wellcome Trust Research Programme, Kilifi, Kenya;Department of Microbiology and Immunology, Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, USA;Respiratory & Meningeal Pathogens Research Unit, University of the Witwatersrand/Medical Research Council, Johannesburg, South Africa;Kenya Medical Research Institute, Wellcome Trust Research Programme, Kilifi, Kenya;Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK;

关键词: Streptococcus pneumoniae;    RSV;    HPIV3;    Gene expression;    Microarray;    Adherence;    Bacterial-viral co-infection;   

DOI  :  10.1186/1471-2164-14-378

 received in 2012-10-10, accepted in 2013-05-24,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundViral upper respiratory tract infections are associated with increased colonization by Streptococcus pneumoniae but the mechanisms underlying this relationship are unclear. The objective of this study is to describe a comprehensive picture of the cellular interaction between the adhering bacteria and host cells in the presence or absence of a viral co-infection.ResultsGene expression profiles of Detroit-562 pharyngeal cells, which were either mock-infected or infected with human respiratory syncytial virus (RSV) or human parainfluenza virus 3 (HPIV3), were analyzed using human microarrays. Transcription response of S. pneumoniae strain TIGR4 (serotype 4) in the presence of either mock- or viral-infected cells was analyzed by pneumococcal microarray. Significantly regulated genes were identified by both significance analysis of microarray (SAM) and a ≥ 2-fold change ratio cut-off. The adherence of S. pneumoniae to human pharyngeal cells was significantly augmented in the presence of RSV or HPIV3 infection. Global gene expression profiling of the host cells during infection with RSV or HPIV3 revealed increased transcription of carcinoembryonic antigen-related cell adhesion molecules (CEACAM1), CD47, fibronectin, interferon-stimulated genes and many other host cell adhesion molecules. Pneumococci increased transcription of several genes involved in adhesive functions (psaA, pilus islet), choline uptake and incorporation (lic operon), as well as transport and binding.ConclusionsWe have identified a core transcriptome that represents the basic machinery required for adherence of pneumococci to D562 cells infected or not infected with a virus. These bacterial genes and cell adhesion molecules can potentially be used to control pneumococcal adherence occurring secondary to a viral infection.

【 授权许可】

Unknown   
© Kimaro Mlacha et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.