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

IF 2.6 2区生物学 Q3 CELL BIOLOGY

Cellular Microbiology 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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来源期刊

Cellular Microbiology 生物-微生物学

CiteScore

9.70

自引率

0.00%

发文量

审稿时长

3 months

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.