ArticleInfection and immunity1999
Group A Streptococcus induces apoptosis in human epithelial cells.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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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Who cites it
27 citing papers in PubMed, 85 citations in OpenAlex.
- Article
- Sequential development of pathological changes in relation to bacterial loads, apoptosis, and immune responses in experimental infection of Streptococcus dysgalactiae subsp. equisimilis (SDSE) in Swiss albino mice.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025Article
- The intricate pathogenicity of Group AVirulence · 2024Review
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- First Report of Genetic Variability ofPathogens (Basel, Switzerland) · 2021Article
- Evaluation of IL-17D in Host Immunity to Group AJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Group AMicrobiology spectrum · 2019Article
- Streptococcal pyrogenic exotoxin B inhibits apoptotic cell clearance by macrophages through protein S cleavage.Scientific reports · 2016Article
- Streptolysin S Promotes Programmed Cell Death and Enhances Inflammatory Signaling in Epithelial Keratinocytes during Group A Streptococcus Infection.Infection and immunity · 2015Article
- Molecular and genomic characterization of pathogenic traits of group A Streptococcus pyogenes.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2015Review
- Endocytosis‒Mediated Invasion and Pathogenicity of Streptococcus agalactiae in Rat Cardiomyocyte (H9C2).PloS one · 2015Article
- Group A Streptococcus Modulates Host Inflammation by Manipulating Polymorphonuclear Leukocyte Cell Death Responses.Journal of innate immunity · 2015Article
- Host responses to group a streptococcus: cell death and inflammation.PLoS pathogens · 2014Review
- Complete Genome Sequence of emm1 Streptococcus pyogenes A20, a Strain with an Intact Two-Component System, CovRS, Isolated from a Patient with Necrotizing Fasciitis.Genome announcements · 2013Article
- Serine/threonine phosphatase (SP-STP), secreted from Streptococcus pyogenes, is a pro-apoptotic protein.The Journal of biological chemistry · 2012Article
- Lactobacilli reduce cell cytotoxicity caused by Streptococcus pyogenes by producing lactic acid that degrades the toxic component lipoteichoic acid.Antimicrobial agents and chemotherapy · 2011Article
- Dextromethorphan efficiently increases bactericidal activity, attenuates inflammatory responses, and prevents group a streptococcal sepsis.Antimicrobial agents and chemotherapy · 2011Article
- Streptococcus adherence and colonization.Microbiology and molecular biology reviews : MMBR · 2009Review
- Streptolysin O promotes group A Streptococcus immune evasion by accelerated macrophage apoptosis.The Journal of biological chemistry · 2009Article
- CD46 Contributes to the severity of group A streptococcal infection.Infection and immunity · 2008Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Internalization of group A streptococcus (GAS) by epithelial cells may have a role in causing invasive diseases. The purpose of this study was to examine the fate of GAS-infected epithelial cells. GAS has the ability to invade A-549 and HEp-2 cells. Both A-549 and HEp-2 cells were killed by infection with GAS. Epithelial cell death mediated by GAS was at least in part through apoptosis, as shown by changes in cellular morphology, DNA fragmentation laddering, and propidium iodide staining for hypodiploid cells. A total of 20% of A-549 cells and 11 to 13% of HEp-2 cells underwent apoptosis after 20 h of GAS infection, whereas only 1 to 2% of these cells exhibited spontaneous apoptosis. We further examined whether streptococcal pyrogenic exotoxin B (SPE B), a cysteine protease produced by GAS, was involved in the apoptosis of epithelial cells. The speB isogenic mutants had less ability to induce cell death than wild-type strains. When A-549 cells were cocultured with the mutant and SPE B for 2 h, the percentage of apoptotic cells did not increase although the number of intracellular bacteria increased to the level of wild-type strains. In addition, apoptosis was blocked by cytochalasin D treatment, which interfered with cytoskeleton function. The caspase inhibitors Z-VAD.FMK, Ac-YVAD.CMK, and Ac-DEVD.FMK inhibited GAS-induced apoptosis. These results demonstrate for the first time that GAS induces apoptosis of epithelial cells and internalization is required for apoptosis. The caspase pathway is involved in GAS-induced apoptosis, and the expression of SPE B in the cells enhances apoptosis.
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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.