NLRP inflammasomes and induced skin inflammation, barrier recovery and extended skin hydration

Gruber, James V.; Stojkoska, V

doi:10.1111/ics.12588

Cited by 4 publications

(8 citation statements)

References 16 publications

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“…Gruber et al suggested that the three ingredients blend and can affect in vitro inflammaging by modulating the expression of active Caspase-1 in inflammasome-activated NHEK, which are key to the process of inflammaging by triggering the release of reservoirs of IL-1 and IL-18, leading later to a release of T cells and dendritic immune response cells. The authors pointed out that these results need to be confirmed by long-term studies [25]. Vollono et al's article reviewing several studies, showed that a potential anti-inflammatory and anti-oxidant effect could be achieved by topical use of curcumin, which may be due to its ability to reduce levels of TNF-α by activated macrophages, inhibit phosphorylase kinase, reduce the number of IL-17A, IL-17F, IL-22 and other pro-inflammatory cytokines, a high level of which has been observed in diseases with underlying inflammaging processes [8].…”

Section: Factors That Inhibit Inflammagingmentioning

confidence: 98%

“…oligomeric α-Synuclein [28] UV radiation [9][10][11][12][13]19,27,29] PM [10,11,21,23] ROS/oxidative stress [10][11][12][13]15,21,27] tobacco extract [11,21] excessive nutrient supply [12] living in urban areas [21] three ingredient blends (probably only in vitro, need more long-term studies) [25] bakuchiol and vanilla tahitensis extract [30] curcumin [8,21] aloe vera topically [21] resveratrol [21] AdipoRon [22] topical nanoemulsion formulation containing tocotrienol-rich fraction [9] Centella asiatica extract [26] estrogen [24] rapamycin topically (potentially) [10] (in [14] no beneficial effects) metformin topically [10,14] emollients/moisturizers (preventing epidermal disruption) [16] seaweed extract (Laminaria Japonica) [17] microbiota (i.e., skin, gut) [6,[13][14][15] epidermal function (dysfunction pro-inflammaging, normal function anti-inflammaging)…”

Section: Factors Accelerating Inflammaging Factors Slowing Down Infla...mentioning

confidence: 99%

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Inflammaging and Immunosenescence as Part of Skin Aging—A Narrative Review

Pająk

Nowicka

Szepietowski

2023

IJMS

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Inflammaging and immunosenescence are associated with aging of the human body, but there are key differences between them. Immunosenescence aims to adapt the body systems to aging, while inflammaging is considered a consequence of immunosenescence. There has been much research in the area of immunosenescence and inflammaging recently, yet our understanding of aging and the ability to develop interventions to decrease the harmful effect of aging on the human body is insufficient. This review is focused on immunosenescence and inflammaging processes in the skin. We aimed to identify factors that influence inflammaging, skin aging, and their mechanisms. We discussed the role of triggering factors (e.g., UV radiations, changes in bioavailability of nitric oxide, senescence-associated secretory phenotype factors, and reactive oxygen species) and inhibiting factors that can potentially be used as anti-aging treatments, as well as the idea of geroprotectors and senotherapeutics. We concluded that while knowledge on external factors can help people to improve their health conditions, knowledge on biochemical factors can help researchers to understand inflammaging process and develop interventions to minimize the impact of aging on the human body. Further research is needed to better understand the role of factors that can slow down or accelerate inflammaging.

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Section: Factors That Inhibit Inflammagingmentioning

confidence: 98%

Section: Factors Accelerating Inflammaging Factors Slowing Down Infla...mentioning

confidence: 99%

Inflammaging and Immunosenescence as Part of Skin Aging—A Narrative Review

Pająk

Nowicka

Szepietowski

2023

IJMS

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“…20 In addition, the studies examine the impact of PQQ2Na on the control of NLRP-induced active Caspase-1 release in UVB and ATP-activated NHEKs using previously reported testing procedures. 17,21,22 Like mitochondrial biogenesis, the NLRP-induced inflammasome activation of active Caspase-1 is intimately related to the mitochondrial ROS activity. 23…”

Section: Introductionmentioning

confidence: 99%

Pyrroloquinoline Quinone Disodium (PQQ2Na) Has an NLRP Inflammasome-Induced Caspase-1 Release Influence in UVB-Irradiated but Not ATP-Treated Human Keratinocytes but Has No Influence in Increasing Skin Cell Mitochondrial Biogenesis in Either Human Keratinocytes or Fibroblasts

JV¹,

Holtz²

2022

CCID

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Introduction Pyrroloquinoline quinone is a bacterial-derived redox factor that has been shown to have numerous benefits in humans. Recently, a model for examining the ability of normal human epidermal keratinocytes (NHEKs) to demonstrate anti-inflammatory benefits via nod-like receptor protein (NLRP)-activated caspase-1 release was reported. The question of whether PQQ2Na might have anti-inflammatory benefits that function through NLRP-activated release of active caspase-1 has not been explored. In addition, it has been reported that PQQ2Na will induce mitochondrial biogenesis in humans when taken orally. Whether or not this effect occurs in skin cells is presently unknown. Methods The inflammation studies followed previously published methods that demonstrated both UVB and ATP were able to upregulate the NLRP-activated release of caspase-1 in NHEKs. In addition, NHEK and normal dermal human fibroblasts (NHDF) were treated with PQQ2Na to see if the molecule might stimulate mitochondrial biogenesis measured by increased expression of cyclooxygenase-1 (COX-1) and succinate dehydrogenase complex, subunit A (SDHA). Results At non-cytotoxic concentrations between 5 µg/mL and 100 µg/mL in NHEKs and between 0.1 µg/mL and 5 µg/mL in fibroblasts, the PQQ2Na had no influence on cellular mitochondrial biogenesis. In ATP-activated NHEKs at concentrations of PQQ2Na between 0.05 µg/mL and 50 µg/mL, there was no influence of PQQ2Na on release of active caspase-1. In NHEKs irradiated with 60mJ/cm 2 of UVB radiation as previously described and treated with 0.05 µg/mL to 50 µg/mL of PQQ2Na, the molecule showed a dose-dependent benefit at reducing the expression of active caspase-1 in the irradiated cells. Discussion Benefits of PQQ2Na on various skin cell types which had not been investigated previously were addressed. Surprisingly, the PPQ2Na had no apparent influence on skin cell mitochondrial biogenesis. However, the molecule has a strong suppressing influence on UVB-induced active caspase-1 release in UVB-irradiated NHEKs.

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“…CBD Isolate typically has a Cannabidiol purity of greater than 99% with no residual Tetrahydrocannabinol (THC). Recently, a model for examining NLRP inflammasome‐activated release of active caspase‐1 in UVB and ATP‐activated Normal Human Epidermal Keratinocytes (NHEK) was reported [12–14]. This model allows for direct examination of the impact of topical treatments on activated NHEKs through measurement of release of active caspase‐1 (ACasp‐1).…”

Section: Introductionmentioning

confidence: 99%

Purified Cannabidiol isolate does not inhibit active caspase‐1 release in NLRP inflammasome‐mediated UVB or ATP‐activated keratinocytes or appear to reduce key inflammatory cytokines in UVB‐irradiate keratinocytes

Gruber

Holtz

2021

Intern J of Cosmetic Sci

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Background Cannabidiol is a plant‐derived cannabinoid that has been suggested to have several human health benefits including potential anti‐inflammatory effects. It is now common to find various forms of Cannabidiol, most often referred to as CBD, in nutritional supplements and topical treatments. The mechanisms by which CBD can influence inflammatory pathways in the body, and more particularly in the skin, are presently still unclear. It is known that CBD will bind to cannabinoid receptors, CB1 and CB2, in the body and recent work has shown that in keratinocytes, CBD can regulate inflammation through transcriptional regulation involving the NFƙβ nuclear pathways. The fact that CBD operates through the NFƙβ pathways suggests that, perhaps, the molecule may influence the expression of active caspase‐1 through NLRP inflammasome‐mediated pathways. Methods Recently, work has published demonstrating that Normal Human Epidermal Keratinocytes (NHEKs) can be activated by UVB and ATP to express active caspase‐1 via NLRP inflammasome‐mediated pathways. There was a strong interest to see whether highly purified Cannabidiol Isolate (>99% purity) might function to control release of active caspase‐1 by testing of NHEKs using the previously described models. In addition, NHEKs expression of non‐NLRP inflammasome‐induced inflammation markers including IL‐6, IL‐8 and PGE2 was examined in UVB‐activated NHEKs. Results It was found that purified Cannabidiol Isolate did not influence active caspase‐1 release in either UVB or ATP‐activated NHEKs suggesting the molecule does not influence the NLRP inflammasome pathways. In addition, it was surprisingly found that the Cannabidiol Isolate did not impact the expression of additional UVB‐activated non‐NLRP inflammatory markers. Conclusions Data presented suggest that if Cannabidiol functions as an anti‐inflammatory, it does so through pathways not associated with either the NLRP inflammasome‐mediated expression of caspase‐1 or through the more commonly known expression of interleukin or prostaglandin inflammatory pathways.

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NLRP inflammasomes and induced skin inflammation, barrier recovery and extended skin hydration

Cited by 4 publications

References 16 publications

Inflammaging and Immunosenescence as Part of Skin Aging—A Narrative Review

Inflammaging and Immunosenescence as Part of Skin Aging—A Narrative Review

Pyrroloquinoline Quinone Disodium (PQQ2Na) Has an NLRP Inflammasome-Induced Caspase-1 Release Influence in UVB-Irradiated but Not ATP-Treated Human Keratinocytes but Has No Influence in Increasing Skin Cell Mitochondrial Biogenesis in Either Human Keratinocytes or Fibroblasts

Purified Cannabidiol isolate does not inhibit active caspase‐1 release in NLRP inflammasome‐mediated UVB or ATP‐activated keratinocytes or appear to reduce key inflammatory cytokines in UVB‐irradiate keratinocytes

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