Evidence map›Paper›PMID 17923519›Full record

ArticleInfection and immunity2007

PspA and PspC minimize immune adherence and transfer of pneumococci from erythrocytes to macrophages through their effects on complement activation.

Jie Li, David T Glover, Alexander J Szalai, Susan K Hollingshead, David E Briles

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
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  6. Frontiers in cellular and infection microbiology · 2022
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Effects of Expression ofFrontiers in microbiology · 2021
    Article
  12. Protective responses of an engineered PspA recombinant antigen againstBiotechnology reports (Amsterdam, Netherlands) · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Role of neural barriers in the pathogenesis and outcome ofExperimental and therapeutic medicine · 2017
    Article
  17. Role ofFrontiers in microbiology · 2017
    Review
  18. 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

5 authors at 1 institution in 1 country.

Jie LiDepartment of Microbiology, University of Alabama at Birmingham, AL 35294, USA.
David T Glover
Alexander J Szalai
Susan K Hollingshead
David E Briles
University of Alabama at Birmingham · US

Funding

IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
PspA: A Potential Pneumococcal Vaccine ComponentR01AI021548 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRILES, DAVID E · 1985 to 2012
$6.0M
PspA mechanisms of humoral immunity, functional assays, and optimal vaccine constR56AI021548 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRILES, DAVID E · 2014 to 2014
$543k
NIAID NIH HHS AI21548NIAID NIH HHS R01 AI021548NIAID NIH HHS R56 AI021548NIAID NIH HHS T32 AI007051
6 · The paper itself

Abstract

Pneumococcal surface protein A (PspA) and PspC are important virulence factors. Their absence has been shown to allow improved clearance of pneumococci from the blood of mice and to decrease pneumococcal virulence. In the presence of antibody and complement, pneumococci attach to erythrocytes in a process called immune adherence (IA), which facilitates their delivery to, and eventual phagocytosis by, macrophages. It is not known, however, if PspA and PspC affect IA. Using PspA and/or PspC isogenic mutants and complement-deficient mouse sera, we demonstrated that absence of PspA allows greater deposition of C1q and thus increased classical-pathway-mediated C3 deposition. In the absence of both PspA and PspC, there is also a major increase in C1q-independent C3 deposition through the alternative pathway. The latter was observed even though absence of PspC alone did not have a major effect on alternative-pathway-dependent complement deposition. The enhanced complement C3 deposition realized in the absence of PspA alone and in the absence of PspA and PspC resulted in both greatly increased IA to human erythrocytes and improved transfer of pneumococci from erythrocytes to phagocytes. These data provide new insight into how PspA and PspC act in synergy to protect pneumococci from complement-dependent clearance during invasive infection.

Indexed as

AnimalsBacterial ProteinsCell AdhesionCell LineComplement ActivationComplement C3ErythrocytesHumansImmune Adherence ReactionMacrophagesMiceMice, Inbred C57BLPhagocytosisStreptococcus pneumoniaeVirulence FactorsBacterial ProteinsComplement C3pneumococcal surface protein ASpsA protein, Streptococcus pneumoniaeVirulence Factors

Identifiers

PMID17923519
PMCPMC2168335
OpenAlexW2167678554

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.