ArticleThe Journal of biological chemistry2014
Streptococcus pneumoniae phosphoglycerate kinase is a novel complement inhibitor affecting the membrane attack complex formation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Motif-guided trafficking of leishmanial PAS domain-containing phosphoglycerate kinase into glycosomes and lysosomes.FEBS letters · 2026Article
- Complement C9 deficiency as a novel risk factor for invasive Candida esophagitis in children: a single case in-depth analysis.BMC pediatrics · 2026Article
- Future Pneumococcal Vaccines: Shifting from Capsular Polysaccharides to Protein-Based Immunogens.Vaccines · 2026Review
- Review
- Microbiome and Metaproteome of Craniofacial Implant Regions in Health and Disease.Oral diseases · 2025Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- Microbial evasion of the complement system: a continuous and evolving story.Frontiers in immunology · 2023Review
- Review
- A journey through thePeerJ · 2021Article
- Complement Evasion Strategies of Human Pathogenic Bacteria.Indian journal of microbiology · 2020Review
- Common Genetic Variants in the Complement System and their Potential Link with Disease Susceptibility and Outcome of Invasive Bacterial Infection.Journal of innate immunity · 2020Review
- Why Do Intravascular Schistosomes Coat Themselves in Glycolytic Enzymes?BioEssays : news and reviews in molecular, cellular and developmental biology · 2019Article
- Review
- Article
- Bacterial-Host Interactions: Physiology and Pathophysiology of Respiratory Infection.Physiological reviews · 2018Review
- Novel Two-Component System of Streptococcus sanguinis Affecting Functions Associated with Viability in Saliva and Biofilm Formation.Infection and immunity · 2018Article
- Antibodies to PcpA and PhtD protect mice against Streptococcus pneumoniae by a macrophage- and complement-dependent mechanism.Human vaccines & immunotherapeutics · 2018Article
- The Surface-Exposed Protein SntA Contributes to Complement Evasion in ZoonoticFrontiers in immunology · 2018Article
- Panel 4: Report of the Microbiology Panel.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2017Review
- Role ofFrontiers in microbiology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Gram-positive bacterium Streptococcus pneumoniae is a major human pathogen that causes infections ranging from acute otitis media to life-threatening invasive disease. Pneumococci have evolved several strategies to circumvent the host immune response, in particular the complement attack. The pneumococcal glycolytic enzyme phosphoglycerate kinase (PGK) is both secreted and bound to the bacterial surface and simultaneously binds plasminogen and its tissue plasminogen activator tPA. In the present study we demonstrate that PGK has an additional role in modulating the complement attack. PGK interacted with the membrane attack complex (MAC) components C5, C7, and C9, thereby blocking the assembly and membrane insertion of MAC resulting in significant inhibition of the hemolytic activity of human serum. Recombinant PGK interacted in a dose-dependent manner with these terminal pathway proteins, and the interactions were ionic in nature. In addition, PGK inhibited C9 polymerization both in the fluid phase and on the surface of sheep erythrocytes. Interestingly, PGK bound several MAC proteins simultaneously. Although C5 and C7 had partially overlapping binding sites on PGK, C9 did not compete with either one for PGK binding. Moreover, PGK significantly inhibited MAC deposition via both the classical and alternative pathway at the pneumococcal surface. Additionally, upon activation plasmin(ogen) bound to PGK cleaved the central complement protein C3b thereby further modifying the complement attack. In conclusion, our data demonstrate for the first time to our knowledge a novel pneumococcal inhibitor of the terminal complement cascade aiding complement evasion by this important pathogen.
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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.