Inflammasome activation and <scp>IL</scp> ‐1β signalling in group A <i>Streptococcus</i> disease
Johanna Richter, Stephan Brouwer, Kate Schroder, Mark J. Walker
Abstract
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.