Johanna Richter, Stephan Brouwer, Kate Schroder, Mark J. Walker
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Inflammasome activation and IL-1β signalling in group A Streptococcus disease
Group A Streptococcus (GAS) is a Gram-positive bacterial pathogen that causes significant morbidity and mortality worldwide. Recent clinical evidence suggests that the inflammatory marker interleukin-1β (IL-1β) plays an important role in GAS disease progression, and presents a potential target for therapeutic intervention. Interaction with GAS activates the host inflammasome pathway to stimulate production and secretion of IL-1β, but GAS can also stimulate IL-1β production in an inflammasome-independent manner. This review highlights progress that has been made in understanding the importance of host cell inflammasomes and IL-1 signalling in GAS disease, and explores challenges and unsolved problems in this host-pathogen interaction.
Take Away
Inflammasome signalling during GAS infection is an emerging field of research.
GAS modulates the NLRP3 inflammasome pathway through multiple mechanisms.
SpeB contributes to IL-1β production independently of the inflammasome pathway.
IL-1β signalling can be host-protective, but also drive severe GAS disease.
期刊介绍：
Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.
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