Evidence map›Paper›PMID 20814187›Full record

ArticleJournal of innate immunity2010

Streptococcal inhibitor of complement promotes innate immune resistance phenotypes of invasive M1T1 group A Streptococcus.

Morgan A Pence, Suzan H M Rooijakkers, Anna L Cogen, Jason N Cole, Andrew Hollands, Richard L Gallo, Victor Nizet

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 4% of its field
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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Tracing the recent evolution of Group AEmerging microbes & infections · 2026
    Review
  3. Comparing virulence profile of dominantInfectious diseases & immunity · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Protein SIC Secreted fromFrontiers in immunology · 2018
    Observational
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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 at 5 institutions in 4 countries.

Morgan A PenceBiomedical Sciences Graduate Program, Department of Pediatrics, University of California San Diego, San Diego, CA 92093-0687, USA.
Suzan H M Rooijakkers
Anna L Cogen
Jason N Cole
Andrew Hollands
Richard L Gallo
Victor Nizet
University of Wollongong · AUInstitute of Biomedical Science · GBPediatrics and Genetics · USUniversity Medical Center Utrecht · NLUniversity of Montana · US

Funding

Training Program in Basic Clinical GeneticsT32GM008666 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAMILTON, BRUCE A · 1998 to 2021
$8.6M
GAS Switch from Colonizing Bacterium to Invasive PathogenR01AI077780 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NIZET, VICTOR · 2008 to 2019
$3.8M
CATHELICIDINS--A MOLECULAR BACTERIOLOGIC APPROACHR21AI048176 · NIAID · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI GALLO, RICHARD L · 2000 to 2001
$420k
NIAID NIH HHS AI48176NIAID NIH HHS AI77780NIAID NIH HHS R01 AI077780NIGMS NIH HHS T32 GM008666
6 · The paper itself

Abstract

Streptococcal inhibitor of complement (SIC) is a highly polymorphic extracellular protein and putative virulence factor secreted by M1 and M57 strains of group A Streptococcus (GAS). The sic gene is highly upregulated in invasive M1T1 GAS isolates following selection of mutations in the covR/S regulatory locus in vivo. Previous work has shown that SIC (allelic form 1.01) binds to and inactivates complement C5b67 and human cathelicidin LL-37. We examined the contribution of SIC to innate immune resistance phenotypes of GAS in the intact organism, using (1) targeted deletion of sic in wild-type and animal-passaged (covS mutant) M1T1 GAS harboring the sic 1.84 allele and (2) heterologous expression of sic in M49 GAS, which does not possess the sic genein its genome. We find that M1T1 SIC production is strongly upregulated upon covS mutation but that the sic gene is not required for generation and selection of covS mutants in vivo. SIC 1.84 bound both human and murine cathelicidins and was necessary and sufficient to promote covS mutant M1T1 GAS resistance to LL-37, growth in human whole blood and virulence in a murine model of systemic infection. Finally, the sic knockout mutant M1T1 GAS strain was deficient in growth in human serum and intracellular macrophage survival. We conclude that SIC contributes to M1T1 GAS immune resistance and virulence phenotypes.

Indexed as

AnimalsBacterial ProteinsBacteriolysisCathelicidinsCell Growth ProcessesCells, CulturedCloning, MolecularGene Expression Regulation, BacterialGene Knockout TechniquesHistidine KinaseHumansImmune EvasionImmunity, InnateIntracellular Signaling Peptides and ProteinsMacrophages, PeritonealMaleBacterial ProteinsCathelicidinsCovS protein, Streptococcus pyogenesHistidine KinaseIntracellular Signaling Peptides and ProteinsSIC protein, Streptococcus

Identifiers

PMID20814187
PMCPMC3219503
OpenAlexW2136646563

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.