Spinal cord NLRP1 inflammasome contributes to dry skin induced chronic itch in mice

Fan, Jun-Juan; Gao, Bo; Song, Ao-Qi; Zhu, Yajing; Zhou, Jun; Li, Weizu; Yin, Yong; Wu, Wen Li

doi:10.1186/s12974-020-01807-3

Cited by 16 publications

(10 citation statements)

References 65 publications

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“…Genetic variations in NLRP1 are also positively associated with a higher susceptibility to psoriasis ( 101 ). Interestingly, higher NLRP1 expression is correlated to dry skin–induced chronic itch in a sex- and age-dependent manner in mice ( 168 ). NLRP1 has recently been implicated in the pathophysiology of IBD by restricting the beneficial butyrate-producing Clostridiales in the gut of the dextran sulphate sodium (DSS)-induced colitis murine model of IBD ( 107 ).…”

Section: Inflammasomes In Chronic Inflammatory Disordersmentioning

confidence: 99%

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

Suryavanshi

Kovalchuk

2021

Front. Immunol.

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Inflammasomes are cytoplasmic inflammatory signaling protein complexes that detect microbial materials, sterile inflammatory insults, and certain host-derived elements. Inflammasomes, once activated, promote caspase-1–mediated maturation and secretion of pro-inflammatory cytokines, interleukin (IL)-1β and IL-18, leading to pyroptosis. Current advances in inflammasome research support their involvement in the development of chronic inflammatory disorders in contrast to their role in regulating innate immunity. Cannabis (marijuana) is a natural product obtained from the Cannabis sativa plant, and pharmacologically active ingredients of the plant are referred to as cannabinoids. Cannabinoids and cannabis extracts have recently emerged as promising novel drugs for chronic medical conditions. Growing evidence indicates the potent anti-inflammatory potential of cannabinoids, especially Δ9-tetrahydrocannabinol (Δ9-THC), cannabidiol (CBD), and synthetic cannabinoids; however, the mechanisms remain unclear. Several attempts have been made to decipher the role of cannabinoids in modulating inflammasome signaling in the etiology of chronic inflammatory diseases. In this review, we discuss recently published evidence on the effect of cannabinoids on inflammasome signaling. We also discuss the contribution of various cannabinoids in human diseases concerning inflammasome regulation. Lastly, in the milieu of coronavirus disease-2019 (COVID-19) pandemic, we confer available evidence linking inflammasome activation to the pathophysiology of COVID-19 suggesting overall, the importance of cannabinoids as possible drugs to target inflammasome activation in or to support the treatment of a variety of human disorders including COVID-19.

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Section: Inflammasomes In Chronic Inflammatory Disordersmentioning

confidence: 99%

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

Suryavanshi

Kovalchuk

2021

Front. Immunol.

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“…The NLRP1 inflammasome is extensively expressed in central nervous system, particularly in neurons and serves as a platform for the recruitment of the apoptosis-associated speck-like protein containing a card (aSc) and procaspase-1 protease. once activated, aSc activates caspase-1 and then induces the processing and maturation of the il-1β, il-6 and il-18 (59). Previous studies have shown that NLRP1 inflammasome is upregulated and accompanied by neuronal damage and cognitive decline in mice model of ad (15).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 alleviates learning and memory impairments and Aβ disposition through inhibiting NLRP1 inflammasome and autophagy dysfunction in APP/PS1 mice

Huang

Kong

et al. 2022

Mol Med Rep

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alzheimer's disease (ad) is a common neurodegenerative disorder. amyloid β (aβ) deposition is considered an important pathological feature of ad. Growing evidence has linked neuroinflammation and autophagy to Aβ deposition in the progression of ad. However, there are few drug options for inhibiting neuroinflammation and autophagy to prevent AD. Ginsenoside rg1 (rg1), a steroidal saponin extracted from ginseng, has been reported to possess multiple neuroprotective effects. The present study aimed to evaluate whether rg1 treatment could attenuate cognitive disorders and neuronal injuries by inhibiting NLRP1 inflammasome and autophagy dysfunction in an ad model of aPP/PS1 mice. The results of behavioral tests indicated that rg1 treatment for 12 weeks could significantly improve olfactory dysfunction as well as learning and memory impairments. The results of histopathological tests indicated that rg1 treatment could reduce aβ deposition and neuronal damages in aPP/PS1-9M mice. additionally, the results of immunoblot, reverse transcription-quantitative Pcr or immunohistochemistry demonstrated that rg1 treatment significantly downregulated the expression levels of inflammation-related proteins of nlrP1, caspase1, il-1β and TnF-α, as well as autophagy-related proteins of p-aMPK/aMPK, Beclin1 and lc3 ii/lc3 i, and increased the expression levels of p-mTor/mTor and P62 in aPP/PS1-9M mice. in addition, the molecular docking analysis showed that there was favorable binding result between rg1 and nlrP1. The present study suggested that rg1 may alleviate learning and memory impairments and aβ disposition by inhibiting NLRP1 inflammasome and improving autophagy dysfunction, suggesting that rg1 may be a potential therapeutic agent for delaying ad.

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“…24 A previous study reported that the spinal cord NOD-like receptor family pyrin domain containing 1 (NLRP1) inflammasome-mediated inflammatory response contributes to dry skin–induced chronic pruritus via the transient receptor potential vanilloid 1 channel and plays an important role in pruritic transmission. 25 NLRP3 belongs to the same family as NLRP1. In addition, increasing evidences show that inflammatory cytokines such as TNF-α, IL-1β and IL-18 are involved in chronic pruritus.…”

Section: Discussionmentioning

confidence: 99%

Alleviating skin barrier disruption, skin inflammation and pruritus: a moisturizing spray containing β-glucan and panthenol

Zhu¹,

Wang²,

Song³

et al. 2022

Int J Dermatol Venereol

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Objective: Inflammatory skin diseases were proved to be associated with dry skin–induced pruritus. However, the relationship between skin inflammation, skin barrier function, and pruritus remains unclarified. The present study aimed to explore this relationship using an acetone–ether–water (AEW) mouse model, and to investigate the anti-itch effects of the combined application of β-glucan and panthenol in a moisturizing spray in this mouse model. Methods: A dry skin–induced chronic pruritus mouse model was established by repeated AEW treatment of the skin. The pruritic behavior, skin barrier function, and expression of molecules related to pruritus and inflammation in topical lesions were measured. The effects of a spray containing β-glucan and panthenol were observed. The t test and one-way analysis of variance were used to evaluate differences between groups. Results: AEW treatment triggered spontaneous scratching with significantly increased numbers of scratching bouts, and disrupted the skin barrier with a significant increase in transepidermal water loss values and a significant decrease in filaggrin gene (FLG) expression (all P < 0.01). AEW treatment also significantly increased the expression of NOD-like receptor family pyrin domain containing 3, apoptosis-associated speck-like protein containing a CARD, caspase-1, interleukin-1β, and tumor necrosis factor-α, as well as the pruritus-associated molecules nerve growth factor, cathepsin S, and thymic stromal lymphopoietin in the skin (all P < 0.01). Application of the spray containing β-glucan and panthenol significantly alleviated these responses, resulting in a reduced number of scratching bouts in 1 hour, reduced transepidermal water loss values, increased filaggrin mRNA expression, and reduced mRNA levels of NOD-like receptor family pyrin domain containing 3, apoptosis-associated speck-like protein containing a CARD, caspase-1, interleukin-1β, tumor necrosis factor-α, cathepsin S, thymic stromal lymphopoietin, and nerve growth factor in skin lesions (all P < 0.05). Conclusion: The present results suggest a relationship between damaged skin barrier function, pruritus, and inflammation. Adding β-glucan and panthenol to moisturizing skincare products may alleviate pruritus induced by dry skin, improve the damaged skin barrier function, and reduce the inflammatory state in local skin areas.

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Spinal cord NLRP1 inflammasome contributes to dry skin induced chronic itch in mice

Cited by 16 publications

References 65 publications

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

Ginsenoside Rg1 alleviates learning and memory impairments and Aβ disposition through inhibiting NLRP1 inflammasome and autophagy dysfunction in APP/PS1 mice

Alleviating skin barrier disruption, skin inflammation and pruritus: a moisturizing spray containing β-glucan and panthenol

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