Evidence map›Paper›PMID 39237647›Full record

ArticleScientific reports2024

Klebsiella LPS O1-antigen prevents complement-mediated killing by inhibiting C9 polymerization.

Frerich M Masson, Salvör Káradóttir, Sjors P A van der Lans, Dennis J Doorduijn, Carla J C de Haas, Suzan H M Rooijakkers, Bart W Bardoel

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Materials today. Bio · 2026
    Article
  9. Article
  10. Epidemiological and Genomic Characteristics ofTransboundary and emerging diseases · 2026
    Article
  11. O-antigen polysaccharides inMicrobiology and molecular biology reviews : MMBR · 2025
    Review
  12. The role of opsonophagocytosis in killing ofCurrent research in microbial sciences · 2025
    Article
  13. Enhanced invasion and survival of antibiotic- resistantFrontiers in cellular and infection microbiology · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Frerich M MassonMedical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Salvör KáradóttirMedical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Sjors P A van der LansMedical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Dennis J DoorduijnMedical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Carla J C de HaasMedical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Suzan H M RooijakkersMedical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Bart W BardoelMedical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands. B.W.Bardoel-2@umcutrecht.nl.

Funding

European Research Council grant agreement no. 101001937, ERC-ACCENTEuropean Union Horizon 2020 research program 787 H2020-EU-ITN-EJD CORVOS #860044Netherlands Organization for Scientific Research (NWO) TTW-NACTAR #16442
6 · The paper itself

Abstract

The Gram-negative bacterium Klebsiella pneumoniae is an important human pathogen. Its treatment has been complicated by the emergence of multi-drug resistant strains. The human complement system is an important part of our innate immune response that can directly kill Gram-negative bacteria by assembling membrane attack complex (MAC) pores into the bacterial outer membrane. To resist this attack, Gram-negative bacteria can modify their lipopolysaccharide (LPS). Especially the decoration of the LPS outer core with the O-antigen polysaccharide has been linked to increased bacterial survival in serum, but not studied in detail. In this study, we characterized various clinical Klebsiella pneumoniae isolates and show that expression of the LPS O1-antigen correlates with resistance to complement-mediated killing. Mechanistic data reveal that the O1-antigen does not inhibit C3b deposition and C5 conversion. In contrast, we see more efficient formation of C5a, and deposition of C6 and C9 when an O-antigen is present. Further downstream analyses revealed that the O1-antigen prevents correct insertion and polymerization of the final MAC component C9 into the bacterial membrane. Altogether, we show that the LPS O1-antigen is a key determining factor for complement resistance by K. pneumoniae and provide insights into the molecular basis of O1-mediated MAC evasion.

Indexed as

Complement C9Klebsiella pneumoniaeO AntigensComplement C3bComplement Membrane Attack ComplexHumansKlebsiella InfectionsLipopolysaccharidesPolymerizationComplement C3bComplement C9Complement Membrane Attack ComplexLipopolysaccharidesO Antigens

Identifiers

PMID39237647
PMCPMC11377433

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Registered trials

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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.