A Dectin-1-Caspase-8 Pathway Licenses Canonical Caspase-1 Inflammasome Activation and Interleukin-1β Release in Response to a Pathogenic Fungus

Ketelut-Carneiro, Natália; Ghosh, Sreya; Levitz, Stuart M.; Fitzgerald, Katherine A.; Silva, João

doi:10.1093/infdis/jix568

Cited by 23 publications

(19 citation statements)

References 50 publications

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“…Here, TLR3/4 engages TRIF (TIR-domain–containing adapter-inducing IFN-β), and TRIF recruits the stress-induced RIP1/FADD/caspase-8 (receptor-interacting protein; FAS-associated death domain) complex, leading to caspase-8 activation (Blander, 2014) and IL-1β/18 maturation (Maelfait et al, 2008; Bossaller et al, 2012; Antonopoulos et al, 2013; Shenderov et al, 2014; Moriwaki et al, 2015). Fungal pathogens detected by dectin-1 can also trigger caspase-8–dependent IL-1β maturation (Ketelut-Carneiro et al, 2018). Here, dectin-1 signaling induces signaling by the CARD9–BCL-10–MALT1 complex to activate caspase-8 (Blander, 2014).…”

Section: Inflammasomes Govern the Maturation Of Il-1β Il-18 And Il-37mentioning

confidence: 99%

Inflammasome signaling and regulation of interleukin-1 family cytokines

Chan

Schroder

2019

Journal of Experimental Medicine

288

208

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Specific IL-1 family cytokines are expressed by cells as cytosolic pro-forms that require cleavage for their activity and cellular release. IL-1β, IL-18, and IL-37 maturation and secretion is governed by inflammatory caspases within signaling platforms called inflammasomes. By inducing pyroptosis, inflammasomes can also drive the release of the alarmin IL-1α. Recent advances have transformed our mechanistic understanding of inflammasome signaling, cell death decisions, and cytokine activation and secretion. Here, we provide an updated view of inflammasome signaling; mechanisms underpinning IL-1α, IL-1β, IL-18, and IL-37 maturation and release; and the functions of these cytokines in protective and pathological inflammation.

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Section: Inflammasomes Govern the Maturation Of Il-1β Il-18 And Il-37mentioning

confidence: 99%

Inflammasome signaling and regulation of interleukin-1 family cytokines

Chan

Schroder

2019

Journal of Experimental Medicine

288

208

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“…Then, these pores promote Ca 2+ unbalance, the pyroptosis, and IL-1β release, as a consequence 25 , 26 . Yet another member of this family of proteases that plays an essential role in programmed cell death, caspase-8, has recently been shown to promote NF-κB activation and induce the synthesis of pro-IL-1β 27 – 29 . The role of Caspase-8 on IL-1β release seems to be more complex as it is also involved in GSDM-D cleavage 30 .…”

Section: Introductionmentioning

confidence: 99%

Caspase-8 mediates inflammation and disease in rodent malaria

et al. 2020

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Earlier studies indicate that either the canonical or non-canonical pathways of inflammasome activation have a limited role on malaria pathogenesis. Here, we report that caspase-8 is a central mediator of systemic inflammation, septic shock in the Plasmodium chabaudi-infected mice and the P. berghei-induced experimental cerebral malaria (ECM). Importantly, our results indicate that the combined deficiencies of caspases-8/1/11 or caspase-8/gasdermin-D (GSDM-D) renders mice impaired to produce both TNFα and IL-1β and highly resistant to lethality in these models, disclosing a complementary, but independent role of caspase-8 and caspases-1/11/GSDM-D in the pathogenesis of malaria. Further, we find that monocytes from malaria patients express active caspases-1, -4 and -8 suggesting that these inflammatory caspases may also play a role in the pathogenesis of human disease.

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“…Similarly, it might be expected that IL-1β could be part of an early and innate response in coccidioidal immunity given its pivotal position as an early mediator of inflammation ( 14 ). With regard to fungal infection, IL-1β has been shown to have a place in a protective murine vaccine against Coccidioides posadasii ( 15 ) as well as in the response to infection with Paracoccidioides brasiliensis ( 16 ) and Candida albicans ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

Ex VivoCytokine Release, Determined by a Multiplex Cytokine Assay, in Response to Coccidioidal Antigen Stimulation of Whole Blood among Subjects with Recently Diagnosed Primary Pulmonary Coccidioidomycosis

Ampel

Robey

Nguyen

et al. 2018

mSphere

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Coccidioidomycosis, commonly known as Valley fever, is a common pneumonia in the southwestern United States. In this paper, we examined the release of 30 inflammatory proteins in whole-blood samples obtained from persons with coccidioidal pneumonia after the blood samples were incubated with a preparation made from the causative fungus, Coccidioides. We found that six of these proteins, all cytokines, were specifically released in high concentrations in these patients. Three of the cytokines were seen very early in disease, and an assay for all six might serve as a marker for the early diagnosis of Valley fever.

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A Dectin-1-Caspase-8 Pathway Licenses Canonical Caspase-1 Inflammasome Activation and Interleukin-1β Release in Response to a Pathogenic Fungus

Abstract: Taken together, these findings revealed an important role for caspase-8 in the innate immune response of host cells to P brasiliensis infection, demonstrating a connected network between noncanonical and canonical inflammasomes to coordinate IL-1β production during fungal challenge.

Cited by 23 publications

References 50 publications

Inflammasome signaling and regulation of interleukin-1 family cytokines

Inflammasome signaling and regulation of interleukin-1 family cytokines

Caspase-8 mediates inflammation and disease in rodent malaria

Ex VivoCytokine Release, Determined by a Multiplex Cytokine Assay, in Response to Coccidioidal Antigen Stimulation of Whole Blood among Subjects with Recently Diagnosed Primary Pulmonary Coccidioidomycosis

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