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Cited by 22Immune Response and InflammationPneumonia and Respiratory InfectionsMicroRNA in disease regulation

Purified Streptococcus pneumoniae Endopeptidase O (PepO) Enhances Particle Uptake by Macrophages in a Toll-Like Receptor 2- and miR-155-Dependent Manner

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Yao, Hua, Zhang, Hong, Lan, Kai, Wang, Hong, Su, Yufeng, Li, Dagen, Song, Zhixin, Cui, Fang +2 more·2017·Infection and Immunity
DOI 10.1128/iai.01012-16PMC PMC5364319
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Abstract

Insights into the host-microbial virulence factor interaction, especially the immune signaling mechanisms, could provide novel prevention and treatment options for pneumococcal diseases. Streptococcus pneumoniae endopeptidase O (PepO) is a newly discovered and ubiquitously expressed pneumococcal virulence protein. A PepO-mutant strain showed impaired adherence to and invasion of host cells compared with the isogenic wild-type strain. It is still unknown whether PepO is involved in the host defense response to pneumococcal infection. Here, we demonstrated that PepO could enhance phagocytosis of Streptococcus pneumoniae and Staphylococcus aureus by peritoneal exudate macrophages (PEMs). Further studies showed that PepO stimulation upregulated the expression of microRNA-155 (miR-155) in PEMs in a time- and dose-dependent manner. PepO-induced enhanced phagocytosis was decreased in cells transfected with an inhibitor of miR-155, while it was increased in cells transfected with a mimic of miR-155. We also revealed that PepO-induced upregulation of miR-155 in PEMs was mediated by Toll-like receptor 2 (TLR2)–NF-κB signaling and that the increased expression of miR-155 downregulated expression of SHIP1. Taken together, these results indicate that PepO induces upregulation of miR-155 in PEMs, contributing to enhanced phagocytosis and host defense response to pneumococci and Staphylococcus aureus .

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  • Streptococcus pneumoniae endopeptidase O upregulates miR-155, enhancing TLR2-mediated phagocytosis.

    “Yao et al. showed that Streptococcus pneumoniae endopeptidase O, a virulence protein, upregulates miR-155 expression enhancing TLR2-mediating phagocytosis [159].”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [159]

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Cited by

Sorted by citations

Authors
Yao, H., Zhang, H., Lan, K., Wang, H., Su, Y., Li, D., Song, Z., Cui, F., Yin, Y., & Zhang, X.
Affiliations
  • Chongqing Medical University (CN)
  • Department of Laboratory Medicine, Key Laboratory of Diagnostic Medicine (Ministry of Education), Chongqing Medical University, Chongqing, People's Republic of China
  • Guangdong Provincial Hospital of Chinese Medicine (CN)
ORCID
Venue
Infection and Immunity
Publisher
American Society for Microbiology
Published
2017-04
Volume
85
Issue
4
ISSN
  • 0019-9567 (ISSN-L)
  • 1098-5522
DOI
10.1128/iai.01012-16
PMC
PMC5364319
OpenAlex
W2588401419
Cited by
22
References
2
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 1 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 1
FWCI
1.36
Type
journal article
Language
en
Open access
Licence
journals.asm.org/non-commercial-tdm-license (tdm)
Locations
  • Infection and Immunity (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • the national natural science fundation grants of china (81371778)
  • the projects of science and technology of chinese ministry of education (V201308)
  • the project of medical scientific research of chongqing (20142004)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Epidemiology › Pneumonia and Respiratory Infections
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
Keywords
Streptococcus pneumoniae, PepO, pneumococcal virulence factors, phagocytosis, macrophages, TLR2, miR-155, NF-κB signaling, SHIP1, Staphylococcus aureus, host defense, host-microbe interactions
MeSH terms
Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases, Animals, Bacterial Proteins, Disease Models, Animal, Gene Expression Regulation, Macrophages, Metalloendopeptidases, Phagocytosis, Pneumococcal Infections, Staphylococcus aureus, Streptococcus pneumoniae, Signal Transduction, Mice, Knockout, RNA Interference, MicroRNAs, Toll-Like Receptor 2, Mice

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