Host responses to group A Streptococcus: cell death and inflammation

Tsatsaronis, James A., Walker, Mark J. and Sanderson-Smith, Martina L. (2014) Host responses to group A Streptococcus: cell death and inflammation. PLoS Pathogens, 10 8: e1004266.1-e1004266.7. doi:10.1371/journal.ppat.1004266

Author Tsatsaronis, James A.
Walker, Mark J.
Sanderson-Smith, Martina L.
Title Host responses to group A Streptococcus: cell death and inflammation
Journal name PLoS Pathogens   Check publisher's open access policy
ISSN 1553-7366
Publication date 2014-08-28
Sub-type Article (original research)
DOI 10.1371/journal.ppat.1004266
Open Access Status DOI
Volume 10
Issue 8
Start page e1004266.1
End page e1004266.7
Total pages 7
Editor Chetan E. Chitnis
Place of publication San Francisco, CA, United States
Publisher Public Library of Science
Collection year 2015
Language eng
Formatted abstract
Infections caused by group A Streptococcus (GAS) are characterized by robust inflammatory responses and can rapidly lead to life-threatening disease manifestations. However, host mechanisms that respond to GAS, which may influence disease pathology, are understudied. Recent works indicate that GAS infection is recognized by multiple extracellular and intracellular receptors and activates cell signalling via discrete pathways. Host leukocyte receptor binding to GAS-derived products mediates release of inflammatory mediators associated with severe GAS disease. GAS induces divergent phagocyte programmed cell death responses and has inflammatory implications. Epithelial cell apoptotic and autophagic components are mobilized by GAS infection, but can be subverted to ensure bacterial survival. Examination of host interactions with GAS and consequences of GAS infection in the context of cellular receptors responsible for GAS recognition, inflammatory mediator responses, and cell death mechanisms, highlights potential avenues for diagnostic and therapeutic intervention. Understanding the molecular and cellular basis of host symptoms during severe GAS disease will assist the development of improved treatment regimens for this formidable pathogen.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Chemistry and Molecular Biosciences
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Citation counts: TR Web of Science Citation Count  Cited 6 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 7 times in Scopus Article | Citations
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Created: Fri, 19 Sep 2014, 10:33:14 EST by Mrs Louise Nimwegen on behalf of School of Chemistry & Molecular Biosciences