ArticleFrontiers in cellular and infection microbiology2016
Streptococcus pneumoniae Endopeptidase O (PepO) Elicits a Strong Innate Immune Response in Mice via TLR2 and TLR4 Signaling Pathways.
Article in Frontiers in cellular and infection microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
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- Combining antibiotic with anti-TLR2/TLR13 therapy prevents brain pathology in pneumococcal meningitis.JCI insight · 2024Article
- The Streptococcus virulence protein PepO triggers anti-tumor immune responses by reprograming tumor-associated macrophages in a mouse triple negative breast cancer model.Cell & bioscience · 2023Article
- Identification and Characterization of Negative Regulators of Rgg1518 Quorum Sensing in Streptococcus pneumoniae.Journal of bacteriology · 2023Article
- Immunoinformatics-aided design of a new multi-epitope vaccine adjuvanted with domain 4 of pneumolysin against Streptococcus pneumoniae strains.BMC bioinformatics · 2023Article
- Host specific adaptations ofCurrent research in microbial sciences · 2023Article
- In silico designing of a novel epitope-based candidate vaccine against Streptococcus pneumoniae with introduction of a new domain of PepO as adjuvant.Journal of translational medicine · 2022Article
- Protein-Based Adjuvants for Vaccines as Immunomodulators of the Innate and Adaptive Immune Response: Current Knowledge, Challenges, and Future Opportunities.Pharmaceutics · 2022Review
- Protease activities of vaginal Porphyromonas species disrupt coagulation and extracellular matrix in the cervicovaginal niche.NPJ biofilms and microbiomes · 2022Article
- Complete Genome Sequencing and Comparative Analysis of the Clinically-DerivedFrontiers in cellular and infection microbiology · 2022Article
- Pathogenicity and virulence ofVirulence · 2021Review
- Extracellular vesicles from methicillin resistantEmerging microbes & infections · 2021Article
- Increased Compulsivity in Adulthood after Early Adolescence Immune Activation: Preclinical Evidence.International journal of environmental research and public health · 2021Article
- Molecular Characterization Based on Whole-Genome Sequencing ofFrontiers in cellular and infection microbiology · 2021Article
- Strategies for Biomaterial-Based Spinal Cord Injury RepairFrontiers in bioengineering and biotechnology · 2021Review
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- Streptococcus pneumoniae aminopeptidase N contributes to bacterial virulence and elicits a strong innate immune response through MAPK and PI3K/AKT signaling.Journal of microbiology (Seoul, Korea) · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interaction between virulence factors of Streptococcus pneumoniae and innate immune receptors elicits host responses through specific signaling pathways during infection. Insights into the signaling events may provide a better knowledge of the starting events for host-pathogen interaction. Here we demonstrated a significant induction of innate immune response elicited by recombinant S. pneumoniae endopeptidase O (rPepO), a newer pneumococcal virulence protein, both in vivo and in vitro. Intratracheal instillation of rPepO protein resulted in significant increase of cytokines production and neutrophils infiltration in mouse lungs. TLR2 or TLR4 deficient mice subjected to rPepO treatment showed decreased cytokines production, reduced neutrophils infiltration and intensified tissue injury as compared with WT mice. Upon stimulation, cytokines TNF-α, IL-6, CXCL1, and CXCL10 were produced by peritoneal exudate macrophages (PEMs) in a TLR2 and TLR4 dependent manner. rPepO-induced cytokines production was markedly decreased in TLR2 or TLR4 deficient PEMs. Further study revealed that cytokines induction relied on the rapid phosphorylation of p38, Akt and p65, not the activation of ERK or JNK. While in TLR2 or TLR4 deficient PEMs the activation of p65 was undetectable. Taken together, these results indicate for the first time that the newer pneumococcal virulence protein PepO activates host innate immune response partially through TLR2 and TLR4 signaling pathways.
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