Inflammasome assembly: The wheels are turning

Brož, Petr

doi:10.1038/cr.2015.137

Cited by 8 publications

(6 citation statements)

References 11 publications

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“…Assembly of inflammasome is unique and its production induces many kinds of exogenous and endogenous signals [ 47 ]. Inflammasome is also thought to have important effects on the regulation of innate adaptive immune response by taking part in the release of the inflammatory cytokines IL-1β and IL-18 which could launch a large number of biological effects [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B (NF-κB) signaling during Haemophilus parasuis infection

et al. 2016

Vet Res

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Haemophilus parasuis (H. parasuis) is the causative agent of Glässer’s disease, a severe membrane inflammation disorder. Previously we showed that Baicalin (BA) possesses anti-inflammatory effects via the NLRP3 inflammatory pathway in an LPS-challenged piglet model. However, whether BA has anti-inflammatory effects upon H. parasuis infection is still unclear. This study investigated the anti-inflammatory effects and mechanisms of BA on H. parasuis-induced inflammatory responses via the NF-κB and NLRP3 inflammasome pathway in piglet mononuclear phagocytes (PMNP). Our data demonstrate that PMNP, when infected with H. parasuis, induced ROS (reactive oxygen species) production, promoted apoptosis, and initiated transcription expression of IL-6, IL-8, IL-10, PGE2, COX-2 and TNF-α via the NF-κB signaling pathway, and IL-1β and IL-18 via the NLRP3 inflammasome signaling pathway. Moreover, when BA was administrated, we observed a reduction in ROS production, suppression of apoptosis, and inhibition of the activation of NF-κB and NLRP3 inflammasome signaling pathway in PMNP treated with H. parasuis. To our best knowledge, this is the first example that uses piglet primary immune cells for an H. parasuis infection study. Our data strongly suggest that BA can reverse the inflammatory effect initiated by H. parasuis and possesses significant immunosuppression activity, which represents a promising therapeutic agent in the treatment of H. parasuis infection.

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Section: Discussionmentioning

confidence: 99%

Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B (NF-κB) signaling during Haemophilus parasuis infection

et al. 2016

Vet Res

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“…In addition to the release of cytokines, inflammasome activation is accompanied by a specific form of cell death called pyroptosis ( Wang et al, 2020 ). Pyroptosis is characterized by Cas1 cleavage of the gasdermin D (GSDMD) protein ( Broz, 2015 ), which leads to cell lysis and subsequent release of cytoplasmic components, including mature forms of IL-1β and IL-18 ( Sansonetti et al, 2000 ).…”

Section: Inflammasome Structurementioning

confidence: 99%

“…NLRP1 was discovered as one of the first in the class of proteins that form inflammasomes ( Kostura et al, 1989 ). It is predominantly expressed by epithelial cells and hematopoietic cells ( Broz, 2015 ). This inflammasome is characterized by the activation of pro-inflammatory proteases, including Cas1 ( Rathinam et al, 2012 ).…”

Section: Inflammasome Activation Mechanismsmentioning

confidence: 99%

Inflammasome Contribution to the Activation of Th1, Th2, and Th17 Immune Responses

et al. 2022

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Inflammasomes are cytosolic polyprotein complexes formed in response to various external and internal stimuli, including viral and bacterial antigens. The main product of the inflammasome is active caspase 1 which proteolytically cleaves, releasing functional interleukin-1 beta (IL-1β) and interleukin-18 (IL-18). These cytokines play a central role in shaping immune response to pathogens. In this review, we will focus on the mechanisms of inflammasome activation, as well as their role in development of Th1, Th2, and Th17 lymphocytes. The contribution of cytokines IL-1β, IL-18, and IL-33, products of activated inflammasomes, are summarized. Additionally, the role of cytokines released from tissue cells in promoting differentiation of lymphocyte populations is discussed.

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“…In this case, NLRC4 is recruited to form the inflammasome following NAIP-mediated detection of the Salmonella flagellin (Fig. 2) (Broz, 2015;Gram et al, 2021). However, it was previously shown that, although NLRC4 recruitment of caspase-1 without ASC does lead to cell death, it also leads to inefficient cytokine processing and secretion (Broz et al, 2010).…”

Section: Activation Of Pyroptosis By Salmonellamentioning

confidence: 97%

“…Salmonella enterica, a Gram-negative bacterium, is the causative agent of gastroenteritis (Bäumler et al, 1998). Research of S. enterica serovar Typhimurium has contributed significantly to the Middle: Following the detection of Salmonella and Shigella by NAIP, NLRC4 is recruited to form the inflammasome (Broz, 2015;Fattinger et al, 2021;Gram et al, 2021;Mitchell et al, 2020). Bottom: IpaH7.8 also targets human gasdermin D (GSDMD) for proteasome degradation and, this way, can block pyroptosis of human but not mouse cells (Luchetti et al, 2021).…”

Section: Pyroptosis In Host Defence Against Salmonella Infectionmentioning

confidence: 99%

Pyroptosis in host defence against bacterial infection

Brokatzky

Mostowy

2022

Disease Models &Amp; Mechanisms

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Pyroptosis, a regulated form of pro-inflammatory cell death, is characterised by cell lysis and by the release of cytokines, damage- and pathogen-associated molecular patterns. It plays an important role during bacterial infection, where it can promote an inflammatory response and eliminate the replicative niche of intracellular pathogens. Recent work, using a variety of bacterial pathogens, has illuminated the versatility of pyroptosis, revealing unexpected and important concepts underlying host defence. In this Review, we overview the molecular mechanisms underlying pyroptosis and discuss their role in host defence, from the single cell to the whole organism. We focus on recent studies using three cellular microbiology paradigms – Mycobacterium tuberculosis, Salmonella Typhimurium and Shigella flexneri – that have transformed the field of pyroptosis. We compare insights discovered in tissue culture, zebrafish and mouse models, highlighting the advantages and disadvantages of using these complementary infection models to investigate pyroptosis and for modelling human infection. Moving forward, we propose that in-depth knowledge of pyroptosis obtained from complementary infection models can better inform future studies using higher vertebrates, including humans, and help develop innovative host-directed therapies to combat bacterial infection.

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Inflammasome assembly: The wheels are turning

Cited by 8 publications

References 11 publications

Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B (NF-κB) signaling during Haemophilus parasuis infection

Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B (NF-κB) signaling during Haemophilus parasuis infection

Inflammasome Contribution to the Activation of Th1, Th2, and Th17 Immune Responses

Pyroptosis in host defence against bacterial infection

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