Evidence map›Paper›PMID 18773116›Full record

ArticlePLoS pathogens2008

PerR confers phagocytic killing resistance and allows pharyngeal colonization by group A Streptococcus.

Ioannis Gryllos, Renata Grifantini, Annalisa Colaprico, Max E Cary, Anders Hakansson, David W Carey, Maria Suarez-Chavez, Leslie A Kalish, Paul D Mitchell, Gary L White and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  6. Article
  7. Article
  8. Pathogens (Basel, Switzerland) · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Structure and function of theThe Journal of biological chemistry · 2018
    Article
  14. The PerR-Regulated PInfection and immunity · 2017
    Article
  15. Article
  16. Article
  17. Stress Physiology of Lactic Acid Bacteria.Microbiology and molecular biology reviews : MMBR · 2016
    Review
  18. Virulence factors of Streptococcus pyogenes strains from women in peri-labor with invasive infections.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016
    Article
  19. Review
  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

11 authors at 5 institutions in 2 countries.

Ioannis GryllosDivision of Infectious Diseases, Children's Hospital Boston, Massachusetts, United States of America.
Renata Grifantini
Annalisa Colaprico
Max E Cary
Anders Hakansson
David W Carey
Maria Suarez-Chavez
Leslie A Kalish
Paul D Mitchell
Gary L White
Michael R Wessels
University of Oklahoma Health Sciences Center · USBoston Children's Hospital · USHarvard University · USNewron Pharmaceuticals (Italy) · ITNovartis (Italy) · IT

Funding

CORE--BABOON RESEARCH RESOURCE PROGRAMP40RR012317 · NCRR · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI WHITE, GARY L · 1998 to 2011
$13.0M
NCRR NIH HHS 2 P40 RR012317-10NCRR NIH HHS P40 RR012317
6 · The paper itself

Abstract

The peroxide response transcriptional regulator, PerR, is thought to contribute to virulence of group A Streptococcus (GAS); however, the specific mechanism through which it enhances adaptation for survival in the human host remains unknown. Here, we identify a critical role of PerR-regulated gene expression in GAS phagocytosis resistance and in virulence during pharyngeal infection. Deletion of perR in M-type 3 strain 003Sm was associated with reduced resistance to phagocytic killing in human blood and by murine macrophages in vitro. The increased phagocytic killing of the perR mutant was abrogated in the presence of the general oxidative burst inhibitor diphenyleneiodonium chloride (DPI), a result that suggests PerR-dependent gene expression counteracts the phagocyte oxidative burst. Moreover, an isogenic perR mutant was severely attenuated in a baboon model of GAS pharyngitis. In competitive infection experiments, the perR mutant was cleared from two animals at 24 h and from four of five animals by day 14, in sharp contrast to wild-type bacteria that persisted in the same five animals for 28 to 42 d. GAS genomic microarrays were used to compare wild-type and perR mutant transcriptomes in order to characterize the PerR regulon of GAS. These studies identified 42 PerR-dependent loci, the majority of which had not been previously recognized. Surprisingly, a large proportion of these loci are involved in sugar utilization and transport, in addition to oxidative stress adaptive responses and virulence. This finding suggests a novel role for PerR in mediating sugar uptake and utilization that, together with phagocytic killing resistance, may contribute to GAS fitness in the infected host. We conclude that PerR controls expression of a diverse regulon that enhances GAS resistance to phagocytic killing and allows adaptation for survival in the pharynx.

Indexed as

Microbial ViabilityBacterial ProteinsCarbohydrate MetabolismGene Expression ProfilingHumansOxidative StressPharynxRepressor ProteinsStreptococcus pyogenesTranscription FactorsVirulenceBacterial Proteinsperoxide repressor proteinsRepressor ProteinsTranscription Factors

Identifiers

PMID18773116
PMCPMC2518855
OpenAlexW2122478680

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.