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

{"title":"Inflammasome activation and IL-1β signalling in group A Streptococcus disease","authors":"Johanna Richter, Stephan Brouwer, Kate Schroder, Mark J. Walker","doi":"10.1111/cmi.13373","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <p>Group A <i>Streptococcus</i> (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.</p>\n </section>\n \n <section>\n \n <h3> Take Away</h3>\n \n <div>\n <ul>\n \n <li>Inflammasome signalling during GAS infection is an emerging field of research.</li>\n \n <li>GAS modulates the NLRP3 inflammasome pathway through multiple mechanisms.</li>\n \n <li>SpeB contributes to IL-1β production independently of the inflammasome pathway.</li>\n \n <li>IL-1β signalling can be host-protective, but also drive severe GAS disease.</li>\n </ul>\n </div>\n </section>\n </div>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2021-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/cmi.13373","citationCount":"7","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/cmi.13373","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}

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.

Abstract Image

查看原文本刊更多论文

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。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464