ArticleProceedings of the National Academy of Sciences of the United States of America2014
Neisseria meningitidis NalP cleaves human complement C3, facilitating degradation of C3b and survival in human serum.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- Discerning dangerous gain of function: most gain of function (GoF) research does not involve infectious microbes.Frontiers in bioengineering and biotechnology · 2026Review
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Changes in serum TIM-3 and complement C3 expression in workers due to Mn exposure.Frontiers in public health · 2023Article
- Functional and Expressional Analyses Reveal the Distinct Role of Complement Factor I in Regulating Complement System Activation during GCRV Infection inInternational journal of molecular sciences · 2022Article
- The complement system and autoimmune diseases.Chronic diseases and translational medicine · 2022Review
- Edwardsiella tarda TraT is an anti-complement factor and a cellular infection promoter.Communications biology · 2022Article
- The Protease SplB of Staphylococcus aureus Targets Host Complement Components and Inhibits Complement-Mediated Bacterial Opsonophagocytosis.Journal of bacteriology · 2022Article
- Phylogenetic Classification and Functional Review of Autotransporters.Frontiers in immunology · 2022Review
- The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022Review
- Complement C3 and Activated Fragment C3a Are Involved in Complement Activation and Anti-Bacterial Immunity.Frontiers in immunology · 2022Article
- Secreted Autotransporter Toxin (Sat) Mediates Innate Immune System Evasion.Frontiers in immunology · 2022Article
- CipA mediates complement resistance ofFrontiers in immunology · 2022Article
- Molecular Analysis of the Contribution of Alkaline Protease A and Elastase B to the Virulence ofFrontiers in cellular and infection microbiology · 2021Article
- TheVaccines · 2020Article
- Role of the Gonococcal Neisserial Heparin Binding Antigen in Microcolony Formation, and Serum Resistance and Adherence to Epithelial Cells.The Journal of infectious diseases · 2020Article
- Review
- 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
- Structural Basis for Evasion of Nutritional Immunity by the PathogenicFrontiers in microbiology · 2019Review
- NHBA is processed by kallikrein from human saliva.PloS one · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The complement system is a crucial component of the innate immune response against invading bacterial pathogens. The human pathogen Neisseria meningitidis (Nm) is known to possess several mechanisms to evade the complement system, including binding to complement inhibitors. In this study, we describe an additional mechanism used by Nm to evade the complement system and survive in human blood. Using an isogenic NalP deletion mutant and NalP complementing strains, we show that the autotransporter protease NalP cleaves C3, the central component of the complement cascade. The cleavage occurs 4 aa upstream from the natural C3 cleavage site and produces shorter C3a-like and longer C3b-like fragments. The C3b-like fragment is degraded in the presence of the complement regulators (factors H and I), and this degradation results in lower deposition of C3b on the bacterial surface. We conclude that NalP is an important factor to increase the survival of Nm in human serum.
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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.