Rosmarinic acid inhibits poly(I:C)-induced inflammatory reaction of epidermal keratinocytes

Zhou, Mingwei; Jiang, Rihua; Kim, Ki-Duck; Lee, Jin-Hyup; Kim, Chang Deok; Wang, Yin; Lee, Jeung‐Hoon

doi:10.1016/j.lfs.2016.05.023

Cited by 29 publications

(24 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NF-κB, MAPKs and STAT signaling have been reported to participate in nucleotide-fragment-induced inflammatory cytokine expression in several cell types [ 22 , 23 , 24 , 25 , 26 ]; however, limited information is available for these signaling events in keratinocytes upon nucleotide fragment induction [ 18 , 36 ]. According to our results, poly(I:C) induces activation of the studied signaling pathways in a shorter time than poly(dA:dT), and a corresponding shift in cytokine expression peaks was observed.…”

Section: Discussionmentioning

confidence: 99%

“…The basal expression of most inflammatory cytokines is low and is regulated in response to stimuli at the transcriptional level, mediated by transcription factors of the nuclear factor κB (NF-κB), mitogen activated protein kinases (MAPK) and signal transducers of activator of transcription (STAT) signal transduction pathways [ 18 ], which have been reported to participate in nucleotide-induced inflammatory cytokine expression in several cell types [ 23 , 24 , 25 , 26 ]. Poly(I:C) was found to induce NF-κB, p38 and STAT-1 signaling in keratinocytes, whereas, in melanocytes, poly(dA:dT) induces NF-κB, p38 and c-Jun N-terminal kinase (JNK) signaling, which differentially regulates cytokine expression [ 18 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Differential Inflammatory-Response Kinetics of Human Keratinocytes upon Cytosolic RNA- and DNA-Fragment Induction

Danis

Janovák

Gubán

et al. 2018

IJMS

View full text Add to dashboard Cite

Keratinocytes are non-professional immune cells contributing actively to innate immune responses partially by reacting to a wide range of molecular patterns by activating pattern recognition receptors. Cytosolic nucleotide fragments as pathogen- or self-derived trigger factors are activating inflammasomes and inducing anti-viral signal transduction pathways as well as inducing expression of inflammatory cytokines. We aimed to compare the induced inflammatory reactions in three keratinocyte cell types—normal human epidermal keratinocytes, the HaCaT cell line and the HPV-KER cell line—upon exposure to the synthetic RNA and DNA analogues poly(I:C) and poly(dA:dT) to reveal the underlying signaling events. Both agents induced the expression of interleukin-6 and tumor necrosis factor α in all cell types; however, notable kinetic and expression level differences were found. Western blot analysis revealed rapid activation of the nuclear factor κB (NF-κB), mitogen activated protein kinase and signal transducers of activator of transcription (STAT) signal transduction pathways in keratinocytes upon poly(I:C) treatment, while poly(dA:dT) induced slower activation. Inhibition of NF-κB, p38, STAT-1 and STAT-3 signaling resulted in decreased cytokine expression, whereas inhibition of mitogen-activated protein kinase kinase 1/2 (MEK1/2) signaling showed a negative feedback role in both poly(I:C)- and poly(dA:dT)-induced cytokine expression. Based on our in vitro results nucleotide fragments are able to induce inflammatory reactions in keratinocytes, but with different rate and kinetics of cytokine expression, explained by faster activation of signaling routes by poly(I:C) than poly(dA:dT).

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Differential Inflammatory-Response Kinetics of Human Keratinocytes upon Cytosolic RNA- and DNA-Fragment Induction

Danis

Janovák

Gubán

et al. 2018

IJMS

View full text Add to dashboard Cite

show abstract

“…In the aspect of reducing the levels of NLRP3 and ASC and the secretion of activated IL-1b and caspase-1, RosA the inhibited poly (I: C)-induced activation of inflammatory bodies. (Zhou et al, 2016) Type 1 diabetic mice RosA treatment reduced the levels of IL-6, TNF-a and PGE 2 in the liver and the activity of COX-2. RosA might be an effective protective agent against liver damage in diabetes.…”

Section: Mastitismentioning

confidence: 96%

A Review of the Anti-Inflammatory Effects of Rosmarinic Acid on Inflammatory Diseases

et al. 2020

View full text Add to dashboard Cite

Inflammatory diseases are caused by abnormal immune responses and are characterized by an imbalance of inflammatory mediators and cells. In recent years, the antiinflammatory activity of natural products has attracted wide attention. Rosmarinic acid (RosA) is a water-soluble phenolic compound that is an ester of caffeic acid and 3, 4dihydroxyphenyl lactic acid. It is discovered in many plants, like those of the Boraginaceae and Lamiaceae families. RosA has a wide range of pharmacological effects, including antioxidative, anti-apoptotic, anti-tumorigenic, and anti-inflammatory effects. The antiinflammatory effects of RosA have been revealed through in vitro and in vivo studies of various inflammatory diseases like arthritis, colitis, and atopic dermatitis. This article mainly describes the preclinical research of RosA on inflammatory diseases and depicts a small amount of clinical research data. The purpose of this review is to discuss the antiinflammatory effects of RosA in inflammatory diseases and its underlying mechanism.

show abstract

“…Nevertheless, psoriasis cannot be considered uniquely as a T cell-dependent disease [3], as dysregulated cross talk between immune cells and skin-resident keratinocytes is thought to be essential in psoriasis development [4][5][6]. Recent data suggest that keratinocytes also play a pivotal role in triggering early pathogenic events, as well as in sustaining the chronic plaque of psoriasis [7][8][9]. Skin-resident keratinocytes not only act as inducers of innate immune responses in the early phase, they are also involved in adaptive immune responses and serve as a reservoir of inflammatory mediators necessary for sustained psoriatic lesions [3].…”

Section: Introductionmentioning

confidence: 99%

Autophagy Suppresses Toll‐Like Receptor 3‐Mediated Inflammatory Reaction in Human Epidermal Keratinocytes

Jung

Yim

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

Autophagy, one mechanism of programmed cell death, is fundamental to cellular homeostasis. Previous studies have identified autophagy as a novel mechanism by which cytokines control the immune response. However, its precise role in immune-related inflammatory skin diseases such as psoriasis remains unclear. Thus, this study explored the functional role of autophagy in psoriatic inflammation of epidermal keratinocytes. Strong light chain 3 immunoreactivity was observed in epidermal keratinocytes of both human psoriatic lesions and imiquimod-induced mice psoriatic model, and it was readily induced by polycytidylic acid (poly (I:C)), which stimulates Toll-like receptor 3 (TLR3), in human epidermal keratinocytes in vitro. Rapamycin-induced activation of autophagy significantly reduced poly (I:C)-induced inflammatory reaction, whereas, inhibition of autophagy by 3-methyladeine increased that. Our results indicate that the induction of autophagy may attenuate TLR3-mediated immune responses in human epidermal keratinocytes, thus providing novel insights into the mechanisms underlying the development of inflammatory skin diseases including psoriasis.

show abstract

Rosmarinic acid inhibits poly(I:C)-induced inflammatory reaction of epidermal keratinocytes

Cited by 29 publications

References 23 publications

Differential Inflammatory-Response Kinetics of Human Keratinocytes upon Cytosolic RNA- and DNA-Fragment Induction

Differential Inflammatory-Response Kinetics of Human Keratinocytes upon Cytosolic RNA- and DNA-Fragment Induction

A Review of the Anti-Inflammatory Effects of Rosmarinic Acid on Inflammatory Diseases

Autophagy Suppresses Toll‐Like Receptor 3‐Mediated Inflammatory Reaction in Human Epidermal Keratinocytes

Contact Info

Product

Resources

About