A Water-Soluble Extract from Actinidia arguta Ameliorates Psoriasis-Like Skin Inflammation in Mice by Inhibition of Neutrophil Infiltration

Kim, Hyun-keun; Bae, Min Jung; Lim, Seonung; Lee, Wonwoo; Kim, Sun‐Young

doi:10.3390/nu10101399

Cited by 17 publications

(25 citation statements)

References 38 publications

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“…PG102 is a standardized extract from an edible portion of Actinidia arguta . It has been shown to alleviate clinical symptoms of various animal disease models including spontaneous dermatitis, atopic dermatitis, and psoriasis-like skin inflammation [13–15]. Furthermore, an exploratory human clinical study with 90 asymptomatic atopy patients (serum total IgE > 300 IU/mL) has verified significant immunomodulatory effects along with the safety of PG102 [16].…”

Section: Introductionmentioning

confidence: 99%

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PG102 Upregulates IL-37 through p38, ERK, and Smad3 Pathways in HaCaT Keratinocytes

Kim

Lim

Bae

et al. 2019

Mediators of Inflammation

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IL-37 is an immunomodulatory cytokine that suppresses inflammation in various cell types and disease models. However, its role in keratinocytes has not been clearly understood, and there has been no report on the agents that can increase the expression of IL-37 in keratinocytes. In this study, we investigated the effects of silencing IL37 in HaCaT keratinocytes and the molecular mechanisms involved in the upregulation of IL-37 by PG102, a water-soluble extract from Actinidia arguta. It was found that knockdown of IL37 resulted in the augmented expression of antimicrobial peptides (AMPs) in response to cytokine stimulation. PG102 increased the expression of IL-37 at both mRNA and protein levels presumably by enhancing the phosphorylation of Smad3, ERK, and p38. Indeed, when cells were treated with specific inhibitors for these signaling molecules, the expression level of IL-37 was reduced. PG102 also promoted colocalization of phospho-Smad3 and IL-37. Our results suggest that IL-37 inhibits the expression of AMPs and that PG102 upregulates IL-37 through p38, ERK, and Smad3 pathways in HaCaT cells.

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Section: Introductionmentioning

confidence: 99%

“…Furthermore, an exploratory human clinical study with 90 asymptomatic atopy patients (serum total IgE > 300 IU/mL) has verified significant immunomodulatory effects along with the safety of PG102 [16]. Recently, we have reported that PG102 suppresses the expression of AMPs in HaCaT cells stimulated with inflammatory cytokines [15].…”

Section: Introductionmentioning

confidence: 99%

PG102 Upregulates IL-37 through p38, ERK, and Smad3 Pathways in HaCaT Keratinocytes

Kim

Lim

Bae

et al. 2019

Mediators of Inflammation

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“…Notably, the crosstalk between skin‐resident keratinocytes and innate immune cells generates inflammatory and immune circuits responsible for the initiation, progression and persistence of the disease . In psoriatic lesions, the antimicrobial peptide LL‐37 produced by keratinocytes combined with self‐DNA released from injured cells activates dendritic cells and T cells, and subsequently leads to the production of IL‐23, IL‐17A and IL‐22 and the activation of keratinocytes . The activated keratinocytes secrete pro‐inflammatory cytokines and chemokines, leading to the recruitment of neutrophils to the lesional skin .…”

Section: Introductionmentioning

confidence: 99%

“…The activated keratinocytes secrete pro‐inflammatory cytokines and chemokines, leading to the recruitment of neutrophils to the lesional skin . The infiltrated neutrophils can secrete pro‐inflammatory cytokines and form neutrophil extracellular traps (NETs), consequently exacerbating the disease progression . Therefore, the evolving knowledge of the role of innate immunity and the cell‐cell communication in psoriasis has had a significant impact on revealing the mechanism of the pathogenesis of psoriasis and developing new therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

Mannan‐binding lectin promotes keratinocyte to produce CXCL1 and enhances neutrophil infiltration at the early stages of psoriasis

Zeng

Chen

et al. 2019

Experimental Dermatology

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Psoriasis is a chronic, relapsing inflammatory skin disorder. Numerous experimental evidence and therapeutic evidence have shown that the innate immune response is critical for the pathogenesis and development of psoriasis. Mannan‐binding lectin (MBL), a prototypic pattern recognition molecule of the innate immune system, plays an essential role in the host defense against certain infections and also appears to be a major regulator of inflammation. In this study, we investigated the function of MBL on the course of experimental murine imiquimod (IMQ)‐induced psoriasis. Our data showed that MBL‐deficient (MBL−/−) mice exhibited attenuated skin damage characterized by greatly decreased erythema compared with wild‐type control mice during the early stages of IMQ‐induced psoriasis‐like skin inflammation. The reduced skin inflammation in MBL−/− mice was associated with the decreased infiltration of neutrophils. Furthermore, we have determined that MBL deficiency limited the chemokine CXCL1 production from skin keratinocytes upon IMQ stimulation, which might be responsible for the impaired skin recruitment of neutrophils. Additionally, we have provided the data that MBL protein promotes the IMQ‐induced expression of CXCL1 and activation of MAPK/NF‐κB signalling pathway in human keratinocyte HaCaT cells in vitro. In summary, our study revealed an unexpected role of MBL on keratinocyte function in skin, thus offering a new insight into the pathogenic mechanisms of psoriasis.

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“…HaCaT cells are immortalized cells, which are commonly used in the studies relevant to psoriasis (13). To mimic conditions of psoriatic keratinocytes, HaCaT cells were induced with M5 (consisting of IL-17A, IL-22, IL-1alpha, TNF-alpha and Oncostatin M) as previous reported (27). Therefore, we established a cell model of highly proliferative psoriatic keratinocytes via treating HaCaT cells by M5.…”

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confidence: 99%

Diagnostic value of miR-106a-5p in patients with psoriasis and its regulatory role in inflammatory responses

Miao

Tong

et al. 2020

Preprint

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Background: Psoriasis is a multifactorial, recurring, and chronic inflammatory skin disease. This study was designed to explore the potential role of microRNA-106a-5p (miR-106a-5p) in psoriasis.Methods: The expression levels of miR-106a-5p in the serum of psoriasis patients and healthy individuals were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The diagnostic value of miR-106a-5p in serum was evaluated by the receiver operating characteristics curve (ROC). The levels of interleukin-22 (IL-22), interleukin-17A (IL-17A), and tumor necrosis factor-alpha (TNF-alpha) were determined by enzyme-linked immunosorbent assay.Results: The serum expression of miR-106a-5p was found to be up-regulated in psoriasis patients. ROC curve showed that miR-106a-5p had high specificity and sensitivity in the diagnosis of psoriasis. The correlation between the serum expression level of miR-106a-5p and PASI was positive. The relative expression levels of IL-17A, IL-22 and TNF-alpha in serum of psoriasis patients were significantly upregulated compared with that in healthy control, and showed positive association with serum miR-106a-5p levels. Cell experiments demonstrated that upregulation of miR-106a-5p could promote cell proliferation, and the levels of IL-22, IL-17A and TNF-alpha were upregulated significantly in M5-induced HaCaT cells.Conclusion: Considering the novel and vital role in psoriasis progression, miR-106a-5p is expected to be a new potent target for treatment of psoriasis. MiR-106-5p was expected to use for more immunity diseases research and therapy.

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A Water-Soluble Extract from Actinidia arguta Ameliorates Psoriasis-Like Skin Inflammation in Mice by Inhibition of Neutrophil Infiltration

Cited by 17 publications

References 38 publications

PG102 Upregulates IL-37 through p38, ERK, and Smad3 Pathways in HaCaT Keratinocytes

PG102 Upregulates IL-37 through p38, ERK, and Smad3 Pathways in HaCaT Keratinocytes

Mannan‐binding lectin promotes keratinocyte to produce CXCL1 and enhances neutrophil infiltration at the early stages of psoriasis

Diagnostic value of miR-106a-5p in patients with psoriasis and its regulatory role in inflammatory responses

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