A mechanistic insight into curcumin modulation of the IL-1β secretion and NLRP3 S-glutathionylation induced by needle-like cationic cellulose nanocrystals in myeloid cells

Guglielmo, Andrew; Sabra, Adham; Elbery, Mostafa; Cerveira, Milena Mattes; Ghenov, Fernanda; Sunasee, Rajesh; Ckless, Karina

doi:10.1016/j.cbi.2017.06.028

Cited by 41 publications

(26 citation statements)

References 33 publications

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“…Both caspase‐1 and caspase‐3 are negatively regulated by GSH, limiting their proteolytic capabilities . Glutathionylation of NLRP3 has recently been identified in macrophages co‐treated with LPS and curcumin, an anti‐inflammatory compound . Interestingly, the deglutathionylation of NLRP3 was associated with increased interaction of glutathionylated caspase‐1, suggesting the NLRP3 inflammasome assembles in tandem with enzymatically inhibited caspase‐1, possibly to prevent activation of the NLRP3 inflammasome.…”

Section: Redox Sensing In Nlrp3 Activationmentioning

confidence: 99%

Metabolic regulation of NLRP3

Hughes

O’Neill

2017

Immunological Reviews

265

167

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A shift in our understanding of macrophage biology has come about as a result of recent discoveries in the area of metabolic reprogramming of macrophages. The NLRP3 inflammasome drives the activation of caspase-1, leading to the production of IL-1β, IL-18, and a type of cell death termed pyroptosis. The NLRP3 inflammasome has been shown to sense metabolites such as palmitate, uric acid, and cholesterol crystals and is inhibited by ketone bodies produced during metabolic flux. The NLRP3 inflammasome has also been shown to be regulated by mitochondrial reactive oxygen species and components of glycolysis, such as Hexokinase. Here, we review these findings and discuss their importance for inflammation and furthermore discuss potential therapeutic benefits of targeting NLRP3.

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Section: Redox Sensing In Nlrp3 Activationmentioning

confidence: 99%

Metabolic regulation of NLRP3

Hughes

O’Neill

2017

Immunological Reviews

265

167

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“…Several inflammasomes, including NLRP1, NLRP3, NLRC4, and NLRP6, have been studied thus far . The NLR family pyrin domain containing 3 (NLRP3) is relevant for several human allergic disorders because its activation is associated with a range of allergic stimuli, such as silica, alum, and other allergens …”

Section: Nlrp3 Inflammasomementioning

confidence: 99%

NLRP3 inflammasome: A likely target for the treatment of allergic diseases

Xiao

2018

Clin Experimental Allergy

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Allergic diseases, such as asthma, rhinitis, dermatitis, conjunctivitis, and anaphylaxis, have recently become a global public health concern. According to previous studies, the NLRP3 inflammasome is a multi-protein complex known to be associated with many inflammatory conditions. In response to allergens or allergen/damage-associated molecular signals, NLRP3 changes its conformation to allow the assembly of the NLRP3 inflammasome complex and activates caspase-1, which is an evolutionarily conserved enzyme that proteolytically cleaves other proteins, such as the precursors of the inflammatory cytokines IL-1β and IL-18. Subsequently, active caspase-1 cleaves pro-IL-1 and pro-IL-18. Recently, accumulating human and mouse experimental evidence has demonstrated that the NLRP3 inflammasome, IL-1β, and IL-18 are critically involved in the development of allergic diseases. Furthermore, the application of specific NLRP3 inflammasome inhibitors has been demonstrated in animal models. Therefore, these inhibitors may represent potential therapeutic methods for the management of clinical allergic disorders. This review summarizes findings related to the NLRP3 inflammasome and its related factors and concludes that specific NLRP3 inflammasome inhibitors may be potential therapeutic agents for allergic diseases.

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“…Redox regulation by glutathionylation has been demonstrated for several proteins, such as the NRF2 regulator KEAP1 (Kelch-like ECH-associated protein 1) (see below) [30,31], HIF-1α [32], p53 [33], actin, GAPDH [34], mitochondrial thymidine kinase 2 [35], caspase-3 [36,37], caspase-8 [38], caspase-1 [39], NLRP3 [40] and proIL-1β [41]. Moreover, redox regulation by other types of oxidation of redox-sensitive cysteine residues has been described, for example for p62 [42] or caspase-1 [43].…”

Section: Redox Sensing and Redox Regulationmentioning

confidence: 99%

“…Moreover, redox regulation by other types of oxidation of redox-sensitive cysteine residues has been described, for example for p62 [42] or caspase-1 [43]. However, as the analytical detection of modified cysteine residues, particularly by glutathione but also by other molecules, is currently a major challenge in the field, the targeted cysteine residues are often unknown [34,35,38,40] or a matter of debate [36,37].…”

Section: Redox Sensing and Redox Regulationmentioning

confidence: 99%

Electrophiles against (Skin) Diseases: More Than Nrf2

Hennig

Fenini

et al. 2020

Biomolecules

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The skin represents an indispensable barrier between the organism and the environment and is the first line of defense against exogenous insults. The transcription factor NRF2 is a central regulator of cytoprotection and stress resistance. NRF2 is activated in response to oxidative stress by reactive oxygen species (ROS) and electrophiles. These electrophiles oxidize specific cysteine residues of the NRF2 inhibitor KEAP1, leading to KEAP1 inactivation and, subsequently, NRF2 activation. As oxidative stress is associated with inflammation, the NRF2 pathway plays important roles in the pathogenesis of common inflammatory diseases and cancer in many tissues and organs, including the skin. The electrophile and NRF2 activator dimethyl fumarate (DMF) is an established and efficient drug for patients suffering from the common inflammatory skin disease psoriasis and the neuro-inflammatory disease multiple sclerosis (MS). In this review, we discuss possible molecular mechanisms underlying the therapeutic activity of DMF and other NRF2 activators. Recent evidence suggests that electrophiles not only activate NRF2, but also target other inflammation-associated pathways including the transcription factor NF-κB and the multi-protein complexes termed inflammasomes. Inflammasomes are central regulators of inflammation and are involved in many inflammatory conditions. Most importantly, the NRF2 and inflammasome pathways are connected at different levels, mainly antagonistically.

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A mechanistic insight into curcumin modulation of the IL-1β secretion and NLRP3 S-glutathionylation induced by needle-like cationic cellulose nanocrystals in myeloid cells

Cited by 41 publications

References 33 publications

Metabolic regulation of NLRP3

Metabolic regulation of NLRP3

NLRP3 inflammasome: A likely target for the treatment of allergic diseases

Electrophiles against (Skin) Diseases: More Than Nrf2

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