ArticlePLoS pathogens2021
Polymerization of C9 enhances bacterial cell envelope damage and killing by membrane attack complex pores.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Complement factors C3 and C5 as tissue biomarkers for differentiating periprosthetic joint infection from aseptic implant failure.European journal of microbiology & immunology · 2026Article
- Excessive C5 conversion prevents C9 polymerisation and subsequent MAC-dependent killing of Klebsiella pneumoniae.PLoS pathogens · 2026Article
- Complement C9 deficiency as a novel risk factor for invasive Candida esophagitis in children: a single case in-depth analysis.BMC pediatrics · 2026Article
- Plasma Proteomic Profile of Chemotherapy-Induced Severe Neutropenia: A Pilot Discovery Phase Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Bactericidal membrane attack complex formation initiates at the new pole of E. coli.EMBO reports · 2026Article
- The Bacterial Swiss Army Knife: ExPEC Utilizes Multiple Resistance Mechanisms to Counteract Host Immune Responses.Vaccines · 2025Review
- Antibiotic-resistant Acinetobacter baumannii can be killed by a combination of bacteriophages and complement.Medical microbiology and immunology · 2025Article
- O-antigen polysaccharides inMicrobiology and molecular biology reviews : MMBR · 2025Review
- Terminal complement complexes with or without C9 potentiate antimicrobial activity againstmBio · 2025Article
- Acinetobacter baumannii Clinical Isolates Resist Complement-Mediated Lysis by Inhibiting the Complement Cascade and Improperly Depositing MAC.Journal of innate immunity · 2025Article
- Klebsiella LPS O1-antigen prevents complement-mediated killing by inhibiting C9 polymerization.Scientific reports · 2024Article
- Transposon mutagenesis screen ineLife · 2024Article
- Plasmid-encoded toxin ofFrontiers in cellular and infection microbiology · 2024Article
- Artificial surface labelling of Escherichia coli with StrepTagII antigen to study how monoclonal antibodies drive complement-mediated killing.Scientific reports · 2023Article
- The neoepitope of the complement C5b-9 Membrane Attack Complex is formed by proximity of adjacent ancillary regions of C9.Communications biology · 2023Article
- Genome-wide screen in human plasma identifies multifaceted complement evasion of Pseudomonas aeruginosa.PLoS pathogens · 2023Article
- Hepatitis B virus suppresses complement C9 synthesis by limiting the availability of transcription factor USF-1 and inhibits formation of membrane attack complex: implications in disease pathogenesis.Journal of biomedical science · 2022Article
- Expansion and Neofunctionalization of Actinoporin-like Genes in Mediterranean Mussel (Mytilus galloprovincialis).Genome biology and evolution · 2022Article
- Soluble MAC is primarily released from MAC-resistant bacteria that potently convert complement component C5.eLife · 2022Article
- Correction: Polymerization of C9 enhances bacterial cell envelope damage and killing by membrane attack complex pores.PLoS pathogens · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement proteins can form membrane attack complex (MAC) pores that directly kill Gram-negative bacteria. MAC pores assemble by stepwise binding of C5b, C6, C7, C8 and finally C9, which can polymerize into a transmembrane ring of up to 18 C9 monomers. It is still unclear if the assembly of a polymeric-C9 ring is necessary to sufficiently damage the bacterial cell envelope to kill bacteria. In this paper, polymerization of C9 was prevented without affecting binding of C9 to C5b-8, by locking the first transmembrane helix domain of C9. Using this system, we show that polymerization of C9 strongly enhanced damage to both the bacterial outer and inner membrane, resulting in more rapid killing of several Escherichia coli and Klebsiella strains in serum. By comparing binding of wildtype and 'locked' C9 by flow cytometry, we also show that polymerization of C9 is impaired when the amount of available C9 per C5b-8 is limited. This suggests that an excess of C9 is required to efficiently form polymeric-C9. Finally, we show that polymerization of C9 was impaired on complement-resistant E. coli strains that survive killing by MAC pores. This suggests that these bacteria can specifically block polymerization of C9. All tested complement-resistant E. coli expressed LPS O-antigen (O-Ag), compared to only one out of four complement-sensitive E. coli. By restoring O-Ag expression in an O-Ag negative strain, we show that the O-Ag impairs polymerization of C9 and results in complement-resistance. Altogether, these insights are important to understand how MAC pores kill bacteria and how bacterial pathogens can resist MAC-dependent killing.
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Registered trials
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.