Host responses to group a streptococcus: cell death and inflammation.

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 i...

Full description

Bibliographic Details
Main Authors: James A Tsatsaronis, Mark J Walker, Martina L Sanderson-Smith
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-08-01
Series:PLoS Pathogens
Online Access:http://europepmc.org/articles/PMC4148426?pdf=render
id doaj-cd9092f3ed2a4dd787a600e11ed1854b
record_format Article
spelling doaj-cd9092f3ed2a4dd787a600e11ed1854b2020-11-25T01:58:26ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742014-08-01108e100426610.1371/journal.ppat.1004266Host responses to group a streptococcus: cell death and inflammation.James A TsatsaronisMark J WalkerMartina L Sanderson-SmithInfections 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.http://europepmc.org/articles/PMC4148426?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author James A Tsatsaronis
Mark J Walker
Martina L Sanderson-Smith
spellingShingle James A Tsatsaronis
Mark J Walker
Martina L Sanderson-Smith
Host responses to group a streptococcus: cell death and inflammation.
PLoS Pathogens
author_facet James A Tsatsaronis
Mark J Walker
Martina L Sanderson-Smith
author_sort James A Tsatsaronis
title Host responses to group a streptococcus: cell death and inflammation.
title_short Host responses to group a streptococcus: cell death and inflammation.
title_full Host responses to group a streptococcus: cell death and inflammation.
title_fullStr Host responses to group a streptococcus: cell death and inflammation.
title_full_unstemmed Host responses to group a streptococcus: cell death and inflammation.
title_sort host responses to group a streptococcus: cell death and inflammation.
publisher Public Library of Science (PLoS)
series PLoS Pathogens
issn 1553-7366
1553-7374
publishDate 2014-08-01
description 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.
url http://europepmc.org/articles/PMC4148426?pdf=render
work_keys_str_mv AT jamesatsatsaronis hostresponsestogroupastreptococcuscelldeathandinflammation
AT markjwalker hostresponsestogroupastreptococcuscelldeathandinflammation
AT martinalsandersonsmith hostresponsestogroupastreptococcuscelldeathandinflammation
_version_ 1724969682289557504