Linked Life Data

18059492

Source:http://linkedlifedata.com/resource/pubmed/id/18059492

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2007-12-6
pubmed:abstractText
The adherence, internalization and persistence of the human pathogen Streptococcus pyogenes (group A streptococci, GAS) to and within host cells were studied, and the induced responses of the infected epithelial cells were investigated. Next to common cellular responses on GAS infection, many responses of the infected HEp-2 epithelial cells are GAS serotype-specific. Moreover, several cellular responses do not correlate with the actual bacterial numbers adherent, internalized and persistent within the cells or the production of major cytolysins, as demonstrated for cytoskeletal pathways, cytokine release and apoptosis induction in infected cells. Measurement of activated caspases and caspase inhibition experiments uncovered activation of multiple caspase pathways by all GAS serotypes tested (M1, M3, M6 and M18). However, caspase 9 played a central role for M6 infections. During the persistence phase of the interaction, a differential and dynamic behavior of the infecting GAS serotype strains was found. After 14 h of host cell contact, all serotype strains caused host cell damage by virtually equal portions of apoptosis induction and necrosis mechanisms, as revealed by measurements of CK18Asp396/CK18 ratios. Between 14 and 24 h, persisting serotype M1 bacteria pertained this effect, whereas the serotype M6 GAS strain induced a major shift to necrotic mechanisms, and the serotype M3 and M18 GAS strains stimulated less necrosis, but shifted their host cells to apoptosis induction. Together, our study revealed that many cellular responses do not belong to general and uniform pathways, which are exploited by all GAS serotypes, explaining many of the already published discordant results.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1751-7362
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
678-92
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:18059492-Apoptosis, pubmed-meshheading:18059492-Bacterial Adhesion, pubmed-meshheading:18059492-Caspase 8, pubmed-meshheading:18059492-Caspase 9, pubmed-meshheading:18059492-Caspases, pubmed-meshheading:18059492-Cell Line, Tumor, pubmed-meshheading:18059492-Epithelial Cells, pubmed-meshheading:18059492-Gene Expression, pubmed-meshheading:18059492-Humans, pubmed-meshheading:18059492-Interferon-gamma, pubmed-meshheading:18059492-Interleukin-6, pubmed-meshheading:18059492-Interleukin-8, pubmed-meshheading:18059492-L-Lactate Dehydrogenase, pubmed-meshheading:18059492-Necrosis, pubmed-meshheading:18059492-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18059492-Serotyping, pubmed-meshheading:18059492-Streptococcus pyogenes, pubmed-meshheading:18059492-Transcription, Genetic, pubmed-meshheading:18059492-Tumor Necrosis Factor-alpha
pubmed:year
2007
pubmed:articleTitle
Streptococcus pyogenes serotype-dependent and independent changes in infected HEp-2 epithelial cells.
pubmed:affiliation
Department of Medical Microbiology and Hospital Hygiene, Institute of Medical Microbiology, Virology and Hygiene, University Hospital Rostock, Schillingallee 70, Rostock, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't