Evidence map›Paper›PMID 18174338›Full record

ArticleInfection and immunity2008

Degradation of complement 3 by streptococcal pyrogenic exotoxin B inhibits complement activation and neutrophil opsonophagocytosis.

Chih-Feng Kuo, Yee-Shin Lin, Woei-Jer Chuang, Jiunn-Jong Wu, Nina Tsao

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.4field-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

35 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Pentamidine inhibition of streptopain attenuatesbioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  7. Immunomodulating Enzymes fromMicroorganisms · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. IL-33/ST2 Axis Plays a Protective Effect inInternational journal of molecular sciences · 2021
    Article
  13. Pathogens (Basel, Switzerland) · 2021
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Chih-Feng KuoDepartment of Nursing, I-Shou University, Kaohsiung County, Taiwan.
Yee-Shin Lin
Woei-Jer Chuang
Jiunn-Jong Wu
Nina Tsao
I-Shou University · TWNational Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Streptococcal pyrogenic exotoxin B (SPE B), a cysteine protease, is an important virulence factor in group A streptococcus (GAS) infection. The inhibition of phagocytic activity by SPE B may help prevent bacteria from being ingested. In this study, we examined the mechanism SPE B uses to enable bacteria to resist opsonophagocytosis. Using an enzyme-linked immunosorbent assay, we found that SPE B-treated serum impaired the activation of the classical, the lectin, and the alternative complement pathways. In contrast, C192S, a SPE B mutant lacking protease activity, had no effect on complement activation. Further study showed that cleavage of serum C3 by SPE B, but not C192S, blocked zymosan-induced production of reactive oxygen species in neutrophils as a result of decreased deposition of C3 fragments on the zymosan surface. Reconstitution of C3 into SPE B-treated serum unblocked zymosan-mediated neutrophil activation dose dependently. SPE B-treated, but not C192S-treated, serum also impaired opsonization of C3 fragments on the surface of GAS strain A20. Moreover, the amount of C3 fragments on the A20 cell surface, a SPE B-producing strain, was less than that on its isogenic mutant strain, SW507, after opsonization with normal serum. A20 opsonized with SPE B-treated serum was more resistant to neutrophil killing than A20 opsonized with normal serum, and SPE B-mediated resistance was C3 dependent. These results suggest a novel SPE B mechanism, one which degrades serum C3 and enables GAS to resist complement damage and opsonophagocytosis.

Indexed as

Amino Acid SubstitutionBacterial ProteinsComplement ActivationComplement C3ExotoxinsMutant ProteinsNeutrophil ActivationNeutrophilsPhagocytosisReactive Oxygen SpeciesStreptococcus pyogenesBacterial ProteinsComplement C3erythrogenic toxinExotoxinsMutant ProteinsReactive Oxygen Species

Identifiers

PMID18174338
PMCPMC2258837
OpenAlexW2158820310

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.