ArticleMedical microbiology and immunology2006
Streptococcal pyrogenic exotoxin B causes mitochondria damage to polymorphonuclear cells preventing phagocytosis of group A streptococcus.
Article in Medical microbiology and immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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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.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Pentamidine inhibition of streptopain attenuatesMicrobiology spectrum · 2025Article
- Pentamidine inhibition of streptopain attenuatesbioRxiv : the preprint server for biology · 2025Article
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Article
- The detrimental impact of extracellular bacterial proteases on wound healing.International wound journal · 2017Review
- Protease-armed bacteria in the skin.Cell and tissue research · 2013Review
- Determining antibody-binding site of streptococcal pyrogenic exotoxin B to protect mice from group a streptococcus infection.PloS one · 2013Article
- Dispersal of Group A streptococcal biofilms by the cysteine protease SpeB leads to increased disease severity in a murine model.PloS one · 2011Article
- Corruption of innate immunity by bacterial proteases.Journal of innate immunity · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The streptococcal pyrogenic exotoxin B (SpeB) is known to be involved in group A streptococcus (GAS) survival in blood, but the detailed mechanism is not clear. For clarification of this issue, speB isogenic mutants of strains M6 and M49 were constructed by using an integrational plasmid and confirmed by Southern blot analysis. The resistance to phagocytosis of wild-type strains and their speB isogenic mutants was analyzed. The results demonstrated a five-fold increase in phagocytosis of speB mutants compared to that of wild-type strains in whole blood, but no significant difference in plasma. To further clarify whether this effect is due to a functional SpeB protein, recombinant SpeB (r-SpeB) and a SpeB mutant protein lacking proteinase activity (r-C192S) were purified and incubated with a speB mutant in whole blood. The results showed a two- to threefold increase in resistance to phagocytosis when the M6 speB mutant was incubated with r-SpeB, but not with r-C192S. Incubation with the wild-type strain, speB mutant, or the r-SpeB protein did not affect the total cell number of polymorphonuclear (PMN) cells in whole blood under laboratory conditions. However, the PMN cells' mitochondria showed decreasing dehydrogenase activity and loss of membrane potential after r-SpeB treatment. These data indicate that SpeB could cause the mitochondria damage to the PMN cells, preventing immune clearance at an early infectious stage.
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Registered trials
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.