ArticlePLoS pathogens2020
Bacterial killing by complement requires direct anchoring of membrane attack complex precursor C5b-7.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Proteins of the SubB family provide multiple mechanisms of serum resistance inEmerging microbes & infections · 2025Article
- Terminal complement complexes with or without C9 potentiate antimicrobial activity againstmBio · 2025Article
- Complement-mediated killing of Escherichia coli by mechanical destabilization of the cell envelope.The EMBO journal · 2024Article
- Klebsiella LPS O1-antigen prevents complement-mediated killing by inhibiting C9 polymerization.Scientific reports · 2024Article
- Discovery of isoquinoline sulfonamides as allosteric gyrase inhibitors with activity against fluoroquinolone-resistant bacteria.Nature chemistry · 2024Article
- In Vivo Evolution of a Klebsiella pneumoniae Capsule Defect With wcaJ Mutation Promotes Complement-Mediated Opsonophagocytosis During Recurrent Infection.The Journal of infectious diseases · 2024Article
- Artificial surface labelling of Escherichia coli with StrepTagII antigen to study how monoclonal antibodies drive complement-mediated killing.Scientific reports · 2023Article
- Pore-Forming Proteins: From Pore Assembly to Structure by Quantitative Single-Molecule Imaging.International journal of molecular sciences · 2023Review
- Functional assays to evaluate antibody-mediated responses againstFrontiers in cellular and infection microbiology · 2023Review
- Neutrophils activated by membrane attack complexes increase the permeability of melanoma blood vessels.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Soluble MAC is primarily released from MAC-resistant bacteria that potently convert complement component C5.eLife · 2022Article
- Emerging roles of the complement system in host-pathogen interactions.Trends in microbiology · 2022Review
- As in Real Estate, Location Matters: Cellular Expression of Complement Varies Between Macular and Peripheral Regions of the Retina and Supporting Tissues.Frontiers in immunology · 2022Article
- Secondary Complement Deficiency Impairs Anti-Microbial Immunity toFrontiers in immunology · 2022Article
- Functional proteomics identify mannitol metabolism in serum resistance and therapeutic implications inFrontiers in immunology · 2022Article
- Challenges and approaches to studying pore-forming proteins.Biochemical Society transactions · 2021Review
- Polymerization of C9 enhances bacterial cell envelope damage and killing by membrane attack complex pores.PLoS pathogens · 2021Article
- Structural basis of soluble membrane attack complex packaging for clearance.Nature communications · 2021Article
- A morphological transformation in respiratory syncytial virus leads to enhanced complement deposition.eLife · 2021Article
- Surviving Serum: the Escherichia coliInfection and immunity · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
An important effector function of the human complement system is to directly kill Gram-negative bacteria via Membrane Attack Complex (MAC) pores. MAC pores are assembled when surface-bound convertase enzymes convert C5 into C5b, which together with C6, C7, C8 and multiple copies of C9 forms a transmembrane pore that damages the bacterial cell envelope. Recently, we found that bacterial killing by MAC pores requires local conversion of C5 by surface-bound convertases. In this study we aimed to understand why local assembly of MAC pores is essential for bacterial killing. Here, we show that rapid interaction of C7 with C5b6 is required to form bactericidal MAC pores on Escherichia coli. Binding experiments with fluorescently labelled C6 show that C7 prevents release of C5b6 from the bacterial surface. Moreover, trypsin shaving experiments and atomic force microscopy revealed that this rapid interaction between C7 and C5b6 is crucial to efficiently anchor C5b-7 to the bacterial cell envelope and form complete MAC pores. Using complement-resistant clinical E. coli strains, we show that bacterial pathogens can prevent complement-dependent killing by interfering with the anchoring of C5b-7. While C5 convertase assembly was unaffected, these resistant strains blocked efficient anchoring of C5b-7 and thus prevented stable insertion of MAC pores into the bacterial cell envelope. Altogether, these findings provide basic molecular insights into how bactericidal MAC pores are assembled and how bacteria evade MAC-dependent killing.
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Registered trials
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