ArticleInfection and immunity2014
Dynamic changes in the Streptococcus pneumoniae transcriptome during transition from biofilm formation to invasive disease upon influenza A virus infection.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
81 citing papers in PubMed, 113 citations in OpenAlex.
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- Commensal to pathogen switch in Streptococcus pneumoniae is influenced by a thermosensing master regulator.PLoS pathogens · 2025Article
- Effects of influenza A infection on liberation of bacteria from biofilms and inflammatory response in anMicrobiology (Reading, England) · 2025Article
- Epigenetic changes and serotype-specific responses of alveolar type II epithelial cells to Streptococcus pneumoniae in resolving influenza A virus infection.Cell communication and signaling : CCS · 2025Article
- Point mutations in functionally diverse genes are associated with increased natural DNA transformation in multidrug resistant Streptococcus pneumoniae.Nucleic acids research · 2025Article
- Characteristics of adults with influenza A virus pneumonia and co-infections identified by mNGS in Jilin, China during 2024-2025.Frontiers in cellular and infection microbiology · 2025Article
- Nasopharyngeal carriage of Streptococcus pneumoniae among Brazilian children: Interplay with viral co-infection.PloS one · 2025Article
- Comparative analysis of theFrontiers in microbiology · 2025Article
- Respiratory tract barrier dysfunction in viral-bacterial co-infection cases.The Japanese dental science review · 2024Review
- Biological puzzles solved by usingJournal of bacteriology · 2024Review
- Application of biofilm dispersion-based nanoparticles in cutting off reinfection.Applied microbiology and biotechnology · 2024Review
- Human monoclonal antibodies protect against viral-mediated pneumococcal superinfection.Frontiers in immunology · 2024Article
- Biofilm-dispersed pneumococci induce elevated leukocyte and platelet activation.Frontiers in cellular and infection microbiology · 2024Article
- Direct comparison of spatial transcriptional heterogeneity across diverse Bacillus subtilis biofilm communities.Nature communications · 2023Article
- Airway proteolytic control of pneumococcal competence.PLoS pathogens · 2023Article
- Isolation ofArchives of Razi Institute · 2023Article
- The Two-Component System YesMN Promotes Pneumococcal Host-to-Host Transmission and Regulates Genes Involved in Zinc Homeostasis.Infection and immunity · 2023Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Streptococcus pneumoniae is a leading cause of infectious disease globally. Nasopharyngeal colonization occurs in biofilms and precedes infection. Prior studies have indicated that biofilm-derived pneumococci are avirulent. However, influenza A virus (IAV) infection releases virulent pneumococci from biofilms in vitro and in vivo. Triggers of dispersal include IAV-induced changes in the nasopharynx, such as increased temperature (fever) and extracellular ATP (tissue damage). We used whole-transcriptome shotgun sequencing (RNA-seq) to compare the S. pneumoniae transcriptome in biofilms, bacteria dispersed from biofilms after exposure to IAV, febrile-range temperature, or ATP, and planktonic cells grown at 37°C. Compared with biofilm bacteria, actively dispersed S. pneumoniae, which were more virulent in invasive disease, upregulated genes involved in carbohydrate metabolism. Enzymatic assays for ATP and lactate production confirmed that dispersed pneumococci exhibited increased metabolism compared to those in biofilms. Dispersed pneumococci also upregulated genes associated with production of bacteriocins and downregulated colonization-associated genes related to competence, fratricide, and the transparent colony phenotype. IAV had the largest impact on the pneumococcal transcriptome. Similar transcriptional differences were also observed when actively dispersed bacteria were compared with avirulent planktonic bacteria. Our data demonstrate complex changes in the pneumococcal transcriptome in response to IAV-induced changes in the environment. Our data suggest that disease is caused by pneumococci that are primed to move to tissue sites with altered nutrient availability and to protect themselves from the nasopharyngeal microflora and host immune response. These data help explain pneumococcal virulence after IAV infection and have important implications for studies of S. pneumoniae pathogenesis.
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