scholarly journals The Lipoxin Receptor/FPR2 Agonist BML-111 Protects Mouse Skin Against Ultraviolet B Radiation

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2953
Author(s):  
Renata M. Martinez ◽  
Victor Fattori ◽  
Priscila Saito ◽  
Ingrid C. Pinto ◽  
Camilla C. A. Rodrigues ◽  
...  
Keyword(s):  
Cell Activation ◽  
Mouse Skin ◽  
Skin Inflammation ◽  
Skin Aging ◽  
Ultraviolet B ◽  
Mast Cell Activation ◽  
Tnf Α ◽  
Nrf2 Signaling Pathway ◽  
Total Antioxidant ◽  
And Oxidative Stress

Excessive exposure to UV, especially UVB, is the most important risk factor for skin cancer and premature skin aging. The identification of the specialized pro-resolving lipid mediators (SPMs) challenged the preexisting paradigm of how inflammation ends. Rather than a passive process, the resolution of inflammation relies on the active production of SPMs, such as Lipoxins (Lx), Maresins, protectins, and Resolvins. LXA4 is an SPM that exerts its action through ALX/FPR2 receptor. Stable ALX/FPR2 agonists are required because SPMs can be quickly metabolized within tissues near the site of formation. BML-111 is a commercially available synthetic ALX/FPR2 receptor agonist with analgesic, antioxidant, and anti-inflammatory properties. Based on that, we aimed to determine the effect of BML-111 in a model of UVB-induced skin inflammation in hairless mice. We demonstrated that BML-111 ameliorates the signs of UVB-induced skin inflammation by reducing neutrophil recruitment and mast cell activation. Reduction of these cells by BML-111 led to lower number of sunburn cells formation, decrease in epidermal thickness, collagen degradation, cytokine production (TNF-α, IL-1β, IL-6, TGF, and IL-10), and oxidative stress (observed by an increase in total antioxidant capacity and Nrf2 signaling pathway), indicating that BML-111 might be a promising drug to treat skin disorders.

scholarly journals 166 Mast cell activation and oxidative stress may be key factors in pulmonary destruction in Cystic Fibrosis

2006 ◽  
Vol 5 ◽  
pp. S38
Author(s):  
P.O. Schiøtz ◽  
M. Kruhøffer ◽  
P. Ebbesen ◽  
V. Zachar ◽  
H.B. Andersen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cystic Fibrosis ◽  
Mast Cell ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Key Factors ◽  
And Oxidative Stress

TRPV4 is a key driver for mast cell activation in LL37mediated skin inflammation

2017 ◽  
Vol 86 (2) ◽  
pp. e69
Author(s):  
Anna Di_Nardo ◽  
Nicholas Mascarenhas ◽  
Zhenping Wang
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Skin Inflammation ◽  
Mast Cell Activation ◽  
Key Driver

scholarly journals Effects of the Fruit Extract of Tribulus terrestris on Skin Inflammation in Mice with Oxazolone-Induced Atopic Dermatitis through Regulation of Calcium Channels, Orai-1 and TRPV3, and Mast Cell Activation

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Seok Yong Kang ◽  
Hyo Won Jung ◽  
Joo Hyun Nam ◽  
Woo Kyung Kim ◽  
Jong-Seong Kang ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cell ◽  
Calcium Channels ◽  
Cell Activation ◽  
Inflammatory Cells ◽  
Skin Inflammation ◽  
Mast Cell Activation ◽  
Tribulus Terrestris ◽  
Symptom Scores ◽  
Safe Approach

Ethnopharmacological Relevance. In this study, we investigated the effects of Tribulus terrestris fruit (Leguminosae, Tribuli Fructus, TF) extract on oxazolone-induced atopic dermatitis in mice. Materials and Methods. TF extract was prepared with 30% ethanol as solvent. The 1% TF extract with or without 0.1% HC was applied to the back skin daily for 24 days. Results. 1% TF extract with 0.1% HC improved AD symptoms and reduced TEWL and symptom scores in AD mice. 1% TF extract with 0.1% HC inhibited skin inflammation through decrease in inflammatory cells infiltration as well as inhibition of Orai-1 expression in skin tissues. TF extract inhibited Orai-1 activity in Orai-1-STIM1 cooverexpressing HEK293T cells but increased TRPV3 activity in TRPV3-overexpressing HEK293T cells. TF extract decreased β-hexosaminidase release in RBL-2H3 cells. Conclusions. The present study demonstrates that the topical application of TF extract improves skin inflammation in AD mice, and the mechanism for this effect appears to be related to the modulation of calcium channels and mast cell activation. This outcome suggests that the combination of TF and steroids could be a more effective and safe approach for AD treatment.

scholarly journals Borrelia burgdorferiSpirochetes Induce Mast Cell Activation and Cytokine Release

1999 ◽  
Vol 67 (3) ◽  
pp. 1107-1115 ◽  
Author(s):  
Jeffrey Talkington ◽  
Steven P. Nickell
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Cell Types ◽  
Host Cells ◽  
Mast Cell Activation ◽  
Cytokine Release ◽  
Necrosis Factor Alpha ◽  
Tnf Α

ABSTRACT The Lyme disease spirochete, Borrelia burgdorferi, is introduced into human hosts via tick bites. Among the cell types present in the skin which may initially contact spirochetes are mast cells. Since spirochetes are known to activate a variety of cell types in vitro, we tested whether B. burgdorferi spirochetes could activate mast cells. We report here that freshly isolated rat peritoneal mast cells or mouse MC/9 mast cells cultured in vitro with live or freeze-thawed B. burgdorferi spirochetes undergo low but detectable degranulation, as measured by [5-3H] hydroxytryptamine release, and they synthesize and secrete the proinflammatory cytokine tumor necrosis factor alpha (TNF-α). In contrast to findings in previous studies, where B. burgdorferi-associated activity was shown to be dependent upon protein lipidation, mast cell TNF-α release was not induced by either lipidated or unlipidated recombinant OspA. This activity was additionally shown to be protease sensitive and surface expressed. Finally, comparisons of TNF-α-inducing activity in known low-, intermediate-, and high-passage B. burgdorferi B31 isolates demonstrated passage-dependent loss of activity, indicating that the activity is probably plasmid encoded. These findings document the presence in low-passage B. burgdorferi spirochetes of a novel lipidation-independent activity capable of inducing cytokine release from host cells.

Glycolic acid attenuates UVB-induced aquaporin-3, matrix metalloproteinase-9 expression, and collagen degradation in keratinocytes and mouse skin

2019 ◽  
Vol 476 (10) ◽  
pp. 1387-1400 ◽  
Author(s):  
Sheau-Chung Tang ◽  
Lee-Chun Tang ◽  
Chin-Hung Liu ◽  
Pei-Yun Liao ◽  
Ji-Ching Lai ◽  
...  
Keyword(s):  
Glycolic Acid ◽  
Transient Receptor Potential ◽  
Mouse Skin ◽  
Skin Aging ◽  
Ultraviolet B ◽  
Mitogen Activated Protein Kinase ◽  
Transient Receptor Potential Vanilloid ◽  
Type I ◽  
Dorsal Skin ◽  
Aquaporin 3

Abstract Ultraviolet-B exposure causes an inflammatory response, photoaged skin, and degradation of extracellular matrix proteins including collagen and elastin. The regulation of these genes was suggested as an important mechanism to attenuate skin aging. Glycolic acid (GA) is commonly present in fruits and recently used to treat dermatological diseases. We reported that GA slows down cell inflammation and aging caused by UVB. Little is known about GA retarding the skin premature senescence or how to impede these events. To investigate the potential of GA to regulate the expression of MMPs and collagen, GA was topically applied onto human keratinocytes and the C57BL/6J mice dorsal skin. In the present study, we demonstrated that GA reduced UVB-induced type-I procollagen expression and secretory collagen levels. GA reverted and dose-dependently increased the level of aquaporin-3 (AQP3), the expression of which was down-regulated by UVB. The UV-induced MMP-9 level and activity were reduced by GA pre-treatment. Concomitantly, GA reverted mitogen-activated protein kinase (MMP-9) activation and inhibited the extracellular signal-regulated kinase activation (p38, pERK) triggered by UVB. The animal model also presented that GA attenuated the wrinkles caused by UVB on the mouse dorsal skin. Finally, GA triggers the transient receptor potential vanilloid-1 (TRPV-1) channel to initiate the anti-photoaging mechanism in keratinocytes. These findings clearly indicated that the mechanisms of GA promote skin protection against UVB-induced photoaging and wrinkle formation. GA might be an important reagent and more widely used to prevent UVB-induced skin aging.

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