Inflammasome activation and IL-1β signalling in group A Streptococcus disease

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2021-06-21 DOI:10.1111/cmi.13373

Johanna Richter, Stephan Brouwer, Kate Schroder, Mark J. Walker

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引用次数: 7

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.

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A组链球菌病炎症小体激活和IL-1β信号传导

A群链球菌(GAS)是一种革兰氏阳性细菌病原体，在世界范围内引起显著的发病率和死亡率。最近的临床证据表明，炎症标志物白细胞介素-1β (IL-1β)在GAS疾病进展中起重要作用，并提供了治疗干预的潜在靶点。与GAS的相互作用激活宿主炎性小体途径刺激IL-1β的产生和分泌，但GAS也可以以炎性小体独立的方式刺激IL-1β的产生。本文综述了在了解宿主细胞炎症小体和IL-1信号传导在GAS疾病中的重要性方面取得的进展，并探讨了宿主-病原体相互作用中的挑战和未解决的问题。去除GAS感染过程中的炎性小体信号是一个新兴的研究领域。GAS通过多种机制调节NLRP3炎性体通路。SpeB独立于炎性体途径参与IL-1β的产生。IL-1β信号可以保护宿主，但也会导致严重的GAS疾病。

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