Role of inflammasomes/pyroptosis and PANoptosis during fungal infection

Briard, Benoit; Malireddi, R.K. Subbarao; Kanneganti, Thirumala‐Devi

doi:10.1371/journal.ppat.1009358

Cited by 45 publications

(25 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, pretreatment with caspase inhibitors can significantly reduce the release of HMGB1 in experimental sepsis 177 . Unlike apoptosis, pyroptosis is typically triggered by activation of caspase-1 or caspase-11 231 . HMGB1 release is decreased by inhibiting caspase-1 activity during pyroptosis 165 .…”

Section: Passive Release Of Hmgb1mentioning

confidence: 99%

The mechanism of HMGB1 secretion and release

2022

View full text Add to dashboard Cite

High mobility group box 1 (HMGB1) is a nonhistone nuclear protein that has multiple functions according to its subcellular location. In the nucleus, HMGB1 is a DNA chaperone that maintains the structure and function of chromosomes. In the cytoplasm, HMGB1 can promote autophagy by binding to BECN1 protein. After its active secretion or passive release, extracellular HMGB1 usually acts as a damage-associated molecular pattern (DAMP) molecule, regulating inflammation and immune responses through different receptors or direct uptake. The secretion and release of HMGB1 is fine-tuned by a variety of factors, including its posttranslational modification (e.g., acetylation, ADP-ribosylation, phosphorylation, and methylation) and the molecular machinery of cell death (e.g., apoptosis, pyroptosis, necroptosis, alkaliptosis, and ferroptosis). In this minireview, we introduce the basic structure and function of HMGB1 and focus on the regulatory mechanism of HMGB1 secretion and release. Understanding these topics may help us develop new HMGB1-targeted drugs for various conditions, especially inflammatory diseases and tissue damage.

show abstract

Section: Passive Release Of Hmgb1mentioning

confidence: 99%

The mechanism of HMGB1 secretion and release

2022

View full text Add to dashboard Cite

show abstract

“…Another inflammasome-independent pathway involving caspase-8 is important for IL-1β and IL-18 production in response to fungal pathogens ( 100 ). Dectin-1 signals via the tyrosine kinase SYK to induce the formation of a CARD9, Bcl-10, MALT1 and caspase-8 complex which recruits the ASC protein to finally mediate cleavage of pro-IL-1β and -IL-18 ( 100 , 101 ). Active caspase-8 cleaves pro-IL-1β at the same site that caspase-1 does ( 93 ).…”

Section: Inflammasome-independent Production Of Il-1βmentioning

confidence: 99%

Interaction of Mycobacteria With Host Cell Inflammasomes

Rastogi

Briken

2022

Front. Immunol.

View full text Add to dashboard Cite

The inflammasome complex is important for host defense against intracellular bacterial infections. Mycobacterium tuberculosis (Mtb) is a facultative intracellular bacterium which is able to survive in infected macrophages. Here we discuss how the host cell inflammasomes sense Mtb and other related mycobacterial species. Furthermore, we describe the molecular mechanisms of NLRP3 inflammasome sensing of Mtb which involve the type VII secretion system ESX-1, cell surface lipids (TDM/TDB), secreted effector proteins (LpqH, PPE13, EST12, EsxA) and double-stranded RNA acting on the priming and/or activation steps of inflammasome activation. In contrast, Mtb also mediates inhibition of the NLRP3 inflammasome by limiting exposure of cell surface ligands via its hydrolase, Hip1, by inhibiting the host cell cathepsin G protease via the secreted Mtb effector Rv3364c and finally, by limiting intracellular triggers (K+ and Cl- efflux and cytosolic reactive oxygen species production) via its serine/threonine kinase PknF. In addition, Mtb inhibits the AIM2 inflammasome activation via an unknown mechanism. Overall, there is good evidence for a tug-of-war between Mtb trying to limit inflammasome activation and the host cell trying to sense Mtb and activate the inflammasome. The detailed molecular mechanisms and the importance of inflammasome activation for virulence of Mtb or host susceptibility have not been fully investigated.

show abstract

“…A recent finding on PANoptosis (concomitant activation of three autonomous cell deaths: pyroptosis, apoptosis and necroptosis) also identified NLRP3 as one of the indispensable components of PANoptosome ( Figure 1 ). PANoptosis is a programmed cell death (PCD) common in macrophages infected with intracellular pathogens, such as influenza A virus, vesicular stomatitis virus, Listeria monocytogenes , Salmonella enteric serovar Typhimurium , Candida albicans and Aspergillus fumigatus , to circumvent pathogen-mediated inhibition [ 133 , 134 ]. The recognition of pathogens or their products by ZBP1 mediates the assemblage of a cytoplasmic multimeric protein complex, known as PANoptosome, and induces PCD called PANoptosis.…”

Section: Nlrp3 and Nlrc4 Inflammasomesmentioning

confidence: 99%

“…The recognition of pathogens or their products by ZBP1 mediates the assemblage of a cytoplasmic multimeric protein complex, known as PANoptosome, and induces PCD called PANoptosis. This complex comprises NLRP3, ASC, CASP8, RIPK3, CASP6 and Z-DNA binding protein 1 (ZBP1) [ 134 , 135 , 136 ]. ZBP1, which is a DNA-dependent activator of IFN-regulatory factors (DAI) [ 137 ], interacts with NLRP3 inflammasome, and together with CASP8, to form a PANoptosome [ 138 , 139 ].…”

Section: Nlrp3 and Nlrc4 Inflammasomesmentioning

confidence: 99%

Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections

Babamale

Chen

2021

IJMS

View full text Add to dashboard Cite

Cell death is an essential immunological apparatus of host defense, but dysregulation of mutually inclusive cell deaths poses severe threats during microbial and parasitic infections leading to deleterious consequences in the pathological progression of infectious diseases. Nucleotide-binding oligomerization domain (NOD)-Leucine-rich repeats (LRR)-containing receptors (NLRs), also called nucleotide-binding oligomerization (NOD)-like receptors (NLRs), are major cytosolic pattern recognition receptors (PRRs), their involvement in the orchestration of innate immunity and host defense against bacteria, viruses, fungi and parasites, often results in the cleavage of gasdermin and the release of IL-1β and IL-18, should be tightly regulated. NLRs are functionally diverse and tissue-specific PRRs expressed by both immune and non-immune cells. Beyond the inflammasome activation, NLRs are also involved in NF-κB and MAPK activation signaling, the regulation of type I IFN (IFN-I) production and the inflammatory cell death during microbial infections. Recent advancements of NLRs biology revealed its possible interplay with pyroptotic cell death and inflammatory mediators, such as caspase 1, caspase 11, IFN-I and GSDMD. This review provides the most updated information that caspase 8 skews the NLRP3 inflammasome activation in PANoptosis during pathogen infection. We also update multidimensional roles of NLRP12 in regulating innate immunity in a content-dependent manner: novel interference of NLRP12 on TLRs and NOD derived-signaling cascade, and the recently unveiled regulatory property of NLRP12 in production of type I IFN. Future prospects of exploring NLRs in controlling cell death during parasitic and microbial infection were highlighted.

show abstract

Role of inflammasomes/pyroptosis and PANoptosis during fungal infection

Cited by 45 publications

References 74 publications

The mechanism of HMGB1 secretion and release

The mechanism of HMGB1 secretion and release

Interaction of Mycobacteria With Host Cell Inflammasomes

Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections

Contact Info

Product

Resources

About