ArticleInfection and immunity2014
MicroRNA-155 is required for clearance of Streptococcus pneumoniae from the nasopharynx.
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 15 papers.
What it found
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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
15 citing papers in PubMed, 25 citations in OpenAlex.
- Non-coding RNA Networks in Infection.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Delayed Tooth Development and the Impaired Differentiation of Stem/Progenitor Cells in Incisors from Type 2 Diabetes Mice.International journal of molecular sciences · 2024Article
- Review
- Myeloid miR-155 plays a limited role in antibacterial defense during Klebsiella-derived pneumosepsis and is dispensable for lipopolysaccharide- or Klebsiella-induced inflammation in mice.Pathogens and disease · 2023Article
- miRNA-Mediated Priming of Macrophage M1 Differentiation Differs in Gram-Positive and Gram-Negative Settings.Genes · 2022Article
- Modes of action and diagnostic value of miRNAs in sepsis.Frontiers in immunology · 2022Review
- Inhibition of miR‑155‑5p attenuates the valvular damage induced by rheumatic heart disease.International journal of molecular medicine · 2020Article
- Immune Network Modeling Predicts Specific Nasopharyngeal and Peripheral Immune Dysregulation in Otitis-Prone Children.Frontiers in immunology · 2020Article
- MicroRNA expression profiles of bovine monocyte-derived macrophages infected in vitro with two strains of Streptococcus agalactiae.BMC genomics · 2018Article
- MicroRNA-155 attenuates late sepsis-induced cardiac dysfunction through JNK and β-arrestin 2.Oncotarget · 2017Article
- Purified Streptococcus pneumoniae Endopeptidase O (PepO) Enhances Particle Uptake by Macrophages in a Toll-Like Receptor 2- and miR-155-Dependent Manner.Infection and immunity · 2017Article
- Pathogens Use and Abuse MicroRNAs to Deceive the Immune System.International journal of molecular sciences · 2016Review
- Mechanisms of Bacterial Colonization of the Respiratory Tract.Annual review of microbiology · 2015Review
- Regulation of IL-17 in autoimmune diseases by transcriptional factors and microRNAs.Frontiers in genetics · 2015Review
- miRNAs reshape immunity and inflammatory responses in bacterial infection.Signal transduction and targeted therapyArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pneumonia caused by Streptococcus pneumoniae is a major cause of death and an economic burden worldwide. S. pneumoniae is an intermittent colonizer of the human upper respiratory tract, and the ability to control asymptomatic colonization determines the likelihood of developing invasive disease. Recognition of S. pneumoniae by resident macrophages via Toll-like receptor 2 (TLR-2) and the macrophage receptor with collagenous structure (MARCO) and the presence of interleukin-17 (IL-17)-secreting CD4(+) T cells are required for macrophage recruitment and bacterial clearance. Despite the fact that the primary cellular effectors needed for bacterial clearance have been identified, much of the underlying regulatory mechanisms are unknown. Herein, we demonstrate that the small, noncoding RNA microRNA-155 (mir-155) is critical for the effective clearance of S. pneumoniae. Our studies show that mir-155-deficient mice maintain the ability to prevent acute invasive pneumococcal infection but have significantly higher bacterial burdens following colonization, independently of macrophage recognition by TLR-2, MARCO expression, or bactericidal capacity. The observed defects in bacterial clearance parallel reduced IL-17A and gamma interferon CD4(+) T-cell responses in vivo, lower IL-17A mRNA levels in the nasopharynx, and a reduced capacity to induce Th17 cell polarization. Given that knockout mice are also limited in the capacity to generate high-titer S. pneumoniae-specific antibodies, we conclude that mir-155 is a critical mediator of the cellular effectors needed to clear primary and secondary S. pneumoniae colonizations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.