scholarly journals The Role of Fucoidans Isolated from the Sporophylls of Undaria pinnatifida against Particulate-Matter-Induced Allergic Airway Inflammation: Evidence of the Attenuation of Oxidative Stress and Inflammatory Responses

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2869 ◽  
Author(s):  
Kalahe Hewage Iresha Nadeeka Madushani Herath ◽  
Hyo Jin Kim ◽  
Areum Kim ◽  
Chung Eui Sook ◽  
Boo-Yong Lee ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Inflammatory Response ◽  
Airway Inflammation ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Undaria Pinnatifida ◽  
Mast Cell Activation ◽  
Cell Hyperplasia ◽  
Mucus Hypersecretion ◽  
Asthma Symptoms

Ambient particulate matter (PM) is a critical environment pollutant that promotes the onset and aggravation of respiratory diseases such as asthma through airway inflammation and hypersecretion of mucus. In this study, we aimed to identify the effects of fucoidans isolated from sporophylls of Undaria pinnatifida on asthma symptoms such as the inflammatory response and mucus secretion using a mouse model. Balb/c mice, intraperitoneally sensitized with ovalbumin (OVA, 10 μg) dissolved in 200 µL saline and 2 mg Al(OH)3, were exposed to PM (5 mg/m3) for 7 consecutive days. In parallel, along with PM exposure, we orally administrated fucoidans (100, 400 mg/Kg) or prednisone (5 mg/Kg), an anti-inflammatory drug. We found that oral administration of fucoidans significantly attenuated PM-induced lipid peroxidation and infiltration of inflammatory cells like F4/80+ macrophages, Gr-1+ granulocytes, and CD4+ T lymphocytes. Fucoidans also attenuated the level of PM-exacerbated IL-4, a primitive cytokine released in Th2 mediated eosinophilic asthma. This further suppressed mast cell activation, degranulation and IgE synthesis of PM exposed mice. Interestingly, fucoidans attenuated PM-exacerbated mucus hypersecretion and goblet cell hyperplasia. Therefore, our results suggest that fucoidans are effective at alleviating PM-exacerbated allergic asthma symptoms by attenuating the airway inflammatory response and mucus hypersecretion.

scholarly journals Resveratrol Inhibits Particulate Matter-Induced Inflammatory Responses in Human Keratinocytes

2020 ◽  
Vol 21 (10) ◽  
pp. 3446 ◽  
Author(s):  
Jung-Won Shin ◽  
Hyun-Sun Lee ◽  
Jung-Im Na ◽  
Chang-Hun Huh ◽  
Kyung-Chan Park ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Inflammatory Response ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Antioxidant Properties ◽  
Complex Mixture ◽  
Human Keratinocytes ◽  
Receptor Activation ◽  
Air Pollutant ◽  
Cellular Inflammatory Response

Particulate matter (PM), a major air pollutant, is a complex mixture of solid and liquid particles of various sizes. PM has been demonstrated to cause intracellular inflammation in human keratinocytes, and is associated with various skin disorders, including atopic dermatitis, eczema, and skin aging. Resveratrol is a natural polyphenol with strong antioxidant properties, and its beneficial effects against skin changes due to PM remain elusive. Therefore, in the present study, we investigated the effect of resveratrol on PM-induced skin inflammation and attempted to deduce the molecular mechanisms underlying resveratrol’s effects. We found that resveratrol inhibited PM-induced aryl hydrocarbon receptor activation and reactive oxygen species formation in keratinocytes. It also suppressed the subsequent cellular inflammatory response by inhibiting mitogen-activated protein kinase activation. Consequentially, resveratrol reduced PM-induced cyclooxygenase-2/prostaglandin E2 and proinflammatory cytokine expression, including that of matrix metalloproteinase (MMP)-1, MMP-9, and interleukin-8, all of which are known to be central mediators of various inflammatory conditions and aging. In conclusion, resveratrol inhibits the PM-induced inflammatory response in human keratinocytes, and we suggest that resveratrol may have potential for preventing air pollution-related skin problems.

scholarly journals Dnmt3arestrains mast cell inflammatory responses

2017 ◽  
Vol 114 (8) ◽  
pp. E1490-E1499 ◽  
Author(s):  
Cristina Leoni ◽  
Sara Montagner ◽  
Andrea Rinaldi ◽  
Francesco Bertoni ◽  
Sara Polletti ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mast Cell ◽  
Cell Biology ◽  
Dna Methyltransferase ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Mast Cell Activation ◽  
Cell Responses

DNA methylation and specifically the DNA methyltransferase enzyme DNMT3A are involved in the pathogenesis of a variety of hematological diseases and in regulating the function of immune cells. Although altered DNA methylation patterns and mutations inDNMT3Acorrelate with mast cell proliferative disorders in humans, the role of DNA methylation in mast cell biology is not understood. By using mast cells lackingDnmt3a, we found that this enzyme is involved in restraining mast cell responses to acute and chronic stimuli, both in vitro and in vivo. The exacerbated mast cell responses observed in the absence ofDnmt3awere recapitulated or enhanced by treatment with the demethylating agent 5-aza-2′-deoxycytidine as well as by down-modulation ofDnmt1expression, further supporting the role of DNA methylation in regulating mast cell activation. Mechanistically, these effects were in part mediated by the dysregulated expression of the scaffold protein IQGAP2, which is characterized by the ability to regulate a wide variety of biological processes. Altogether, our data demonstrate that DNMT3A and DNA methylation are key modulators of mast cell responsiveness to acute and chronic stimulation.

scholarly journals Quercetin Attenuates Trauma-Induced Heterotopic Ossification by Tuning Immune Cell Infiltration and Related Inflammatory Insult

2021 ◽  
Vol 12 ◽  
Author(s):  
Juehong Li ◽  
Ziyang Sun ◽  
Gang Luo ◽  
Shuo Wang ◽  
Haomin Cui ◽  
...  
Keyword(s):  
Mast Cell ◽  
Heterotopic Ossification ◽  
Cell Activation ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Mast Cell Activation ◽  
Cell Infiltration ◽  
Immune Cell Infiltration ◽  
Dependent Manner

Heterotopic ossification (HO) is one of the most intractable disorders following musculoskeletal injury and is characterized by the ectopic presence of bone tissue in the soft tissue leading to severe loss of function in the extremities. Recent studies have indicated that immune cell infiltration and inflammation are involved in aberrant bone formation. In this study, we found increased monocyte/macrophage and mast cell accumulation during early HO progression. Macrophage depletion by clodronate liposomes and mast cell stabilization by cromolyn sodium significantly impeded HO formation. Therefore, we proposed that the dietary phytochemical quercetin could also suppress immune cell recruitment and related inflammatory responses to prevent HO. As expected, quercetin inhibited the monocyte-to-macrophage transition, macrophage polarization, and mast cell activation in vitro in a dose-dependent manner. Using a murine burn/tenotomy model, we also demonstrated that quercetin attenuated inflammatory responses and HO in vivo. Furthermore, elevated SIRT1 and decreased acetylated NFκB p65 expression were responsible for the mechanism of quercetin, and the beneficial effects of quercetin were reversed by the SIRT1 antagonist EX527 and mimicked by the SIRT agonist SRT1720. The findings in this study suggest that targeting monocyte/macrophage and mast cell activities may represent an attractive approach for therapeutic intervention of HO and that quercetin may serve as a promising therapeutic candidate for the treatment of trauma-induced HO by modulating SIRT1/NFκB signaling.

The effect and mechanism of Modified Guo-Min Decoction and Yu-Ping-Feng Powder on fine particulate matter-induced lung inflammatory injury and airway mucus hypersecretion in rats

2020 ◽  
Author(s):  
Feng Feng ◽  
Changle Zhu ◽  
Yufeng Meng ◽  
Fang Guo ◽  
Cuiling Feng
Keyword(s):  
Particulate Matter ◽  
Lung Injury ◽  
Group Treatment ◽  
Clinical Symptoms ◽  
Fine Particulate Matter ◽  
Cell Hyperplasia ◽  
Mucus Hypersecretion ◽  
Fine Particulate ◽  
Significant Difference ◽  
Airway Mucus

Abstract Background Exposure to fine particulate matter (PM2.5) severely impairs public health. The mechanism of PM2.5-induced lung injury is complex and diverse. Modified Guo-Min Decoction (MGMD) and Yu-Ping-Feng Powder (YPFP) have been found to improve clinical symptoms in respiratory patients during smog weather, but the mechanism remains unclear. This study aimed to investigate the effect and mechanism of YPFP and MGMD against PM2.5-induced lung injury. Methods We established the PM2.5 animal model by intratracheal instilling of PM2.5 suspensions. Rats were administrated MGMD/YPFP/distilled water via gavage every day, and all rats were sacrificed after 28 days. At the end of experiment, BALF and lung tissues were collected. Condition of lung injury, inflammatory cells infiltration, inflammatory cytokines, MUC5AC synthesis and release, and phosphorylation of TLR2-MyD88-NFκB and EGFR-PI3K-AKT signalling pathway were evaluated. Results The results demonstrated that both MGMD and YPFP protected rats from PM2.5-induced damaged structure of lung tissues. The infiltration of neutrophil, monocyte, lymphocyte, and eosinophil was reduced after the treatment of two therapies. The production of pro-inflammatory mediators, MCP-1 and NE, as well as the type2 inflammation-related cytokines, IgE and IL-4, were decreased by MGMD and YPFP. However, the MGMD showed more potent effect on inhibiting IL-4, while YPFP benefited in preventing ICMA-1, IL-1β, and IL-17A. Rare significance was detected in the TLR2-MyD88-NFκB of each group. Treatment with MGMD and YPFP decreased goblet cell hyperplasia and the expressions of MUC5AC. The further investigation demonstrated that YPFP had the effect of simultaneously inhibiting the phosphorylation of PI3K and AKT, whereas MGMD only showed a significant difference in AKT. Conclusions Therefore, both MGMD and YPFP could significantly attenuate PM2.5-induced inflammation of lung and airway mucus hypersecretion. Nevertheless, YPFP had more advantage in preventing type1 inflammation and mucus hypersecretion, while MGMD was more beneficial in reducing type2 inflammation.

Inhibitory effect of taxifolin on mast cell activation and mast cell-mediated allergic inflammatory response

2019 ◽  
Vol 71 ◽  
pp. 205-214 ◽  
Author(s):  
Shunli Pan ◽  
Xiaoxia Zhao ◽  
Ning Ji ◽  
Chen Shao ◽  
Bingjie Fu ◽  
...  
Keyword(s):  
Mast Cell ◽  
Inflammatory Response ◽  
Cell Activation ◽  
Inhibitory Effect ◽  
Mast Cell Activation

scholarly journals TNF-α is crucial for the development of mast cell-dependent colitis in mice

2006 ◽  
Vol 291 (5) ◽  
pp. G969-G976 ◽  
Author(s):  
Anneke Rijnierse ◽  
Andries S. Koster ◽  
Frans P. Nijkamp ◽  
Aletta D. Kraneveld
Keyword(s):  
Mast Cell ◽  
Murine Model ◽  
Tissue Damage ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Mast Cell Activation ◽  
Cell Infiltration ◽  
Tnf Α ◽  
Total Tissue

Inflammatory bowel disease (IBD) describes chronic inflammatory conditions of the gastrointestinal tract, and TNF-α plays a pivotal role in mediating the response. The proinflammatory cytokine TNF-α is rapidly released by mast cells after degranulation. In the present study, we hypothesized TNF-α to be an important player in our recently described mast cell-dependent murine model for IBD. The effect of neutralizing anti-TNF-α MAb was studied on colonic hypersensitivity in mice induced by a skin application of dinitrofluorobenzene (DNFB) followed by an intrarectal challenge with dintrobenzene sulfonic acid. Features of the colonic hypersensitivity response included diarrhea, mast cell infiltration and activation, infiltration of inflammatory cells in the colon, colonic patch hypertrophy, and increased mast cell-derived TNF-α levels in the colon. Anti-TNF-α MAb could effectively abrogate diarrhea in DNFB-sensitized mice 72 h after the challenge. The numbers of colonic patches and total tissue damage scores were reduced by anti-TNF-α MAb treatment in DNFB-sensitized mice 72 h after the challenge. Mast cell infiltration and activation remained unaffected by neutralizing anti-TNF-α MAb. Treatment with the corticosteroid dexamethasone, a frequently used therapeutic treatment in IBD, resulted in a reduction of diarrhea, cellular infiltration, and total tissue damage scores to the same extent as anti-TNF-α MAb. Additionally, dexamethasone treatment could also reduce total TNF-α levels in the colon, mast cell numbers, and mast cell activation in both vehicle- and DNFB-sensitized mice 72 h after the challenge. These findings suggest that TNF-α can play an instrumental role in causing inflammatory responses in the present murine model for IBD downstream from mast cell activation.

Neurogenic inflammation in mice deficient in heparin-synthesizing enzyme

2004 ◽  
Vol 286 (3) ◽  
pp. H884-H888 ◽  
Author(s):  
Tine V. Karlsen ◽  
Vegard V. Iversen ◽  
Erik Forsberg ◽  
Lena Kjellén ◽  
Rolf K. Reed ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Neurogenic Inflammation ◽  
Inflammatory Responses ◽  
Fluid Pressure ◽  
Mouse Skin ◽  
Mast Cell Activation ◽  
Protein Extravasation ◽  
Plasma Protein Extravasation ◽  
Rats And Mice

Mast cell activation, or neurogenic inflammation, is known to induce lowering of interstitial fluid pressure (Pif) and plasma protein extravasation (PPE) in several tissues from both rats and mice. To examine a possible role of connective tissue mast cells (CTMCs) in these inflammatory responses, we used mice with dysfunctional CTMCs due to lack of the N-deacetylase/ N-sulfotransferase-2 enzyme (NDST-2–/–). Pif and PPE were measured after challenge with compound 48/80 (C48/80), and Pif alone was measured after treatment either with capsaicin, substance P (SP), or calcitonin gene-related peptide (CGRP). Measurements of Pif in anesthetized (fentanyl/fluanison and midazolam, 1:1) mice were performed in paw skin with glass capillaries connected to a servo-controlled counterpressure system. PPE was measured with microdialysis by using hollow plasmapheresis fibers (cutoff at 3,000 kDa) placed subcutaneously on the back. Intravenous administration of C48/80 lowered Pif significantly ( P < 0.05) in NDST-2–/– mice (–1.67 ± 0.42 mmHg) compared with vehicle (–0.57 ± 0.17 mmHg) but the lowering was significantly ( P < 0.05) less compared with that of the NDST-2+/+ mice (–2.31 ± 0.47 mmHg). PPE was increased 300% after treatment with C48/80 in NDST-2+/+ mice, whereas there was no increase in PPE in NDST-2–/– mice. Capsaicin, SP, and CGRP lowered Pif significantly ( P < 0.05) compared with vehicle and to the same extent in both NDST-2+/+ and NDST-2–/– mice. We can conclude that although NDST-2–/– mice demonstrate an altered response in Pif after mast cell activation, there was no similar alteration after neurogenic inflammation. Therefore, we suggest that neurogenic inflammation in mouse skin is not exclusively dependent on intact CTMCs.

scholarly journals Intestinal Mucosal Mast Cells: Key Modulators of Barrier Function and Homeostasis

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 135 ◽  
Author(s):  
Mercé Albert-Bayo ◽  
Irene Paracuellos ◽  
Ana M. González-Castro ◽  
Amanda Rodríguez-Urrutia ◽  
María J. Rodríguez-Lagunas ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Cell Activity ◽  
Intestinal Barrier ◽  
The Body ◽  
Mast Cell Activation ◽  
Mucosal Barrier ◽  
Mucosal Mast Cell

The gastrointestinal tract harbours the largest population of mast cells in the body; this highly specialised leukocyte cell type is able to adapt its phenotype and function to the microenvironment in which it resides. Mast cells react to external and internal stimuli thanks to the variety of receptors they express, and carry out effector and regulatory tasks by means of the mediators of different natures they produce. Mast cells are fundamental elements of the intestinal barrier as they regulate epithelial function and integrity, modulate both innate and adaptive mucosal immunity, and maintain neuro-immune interactions, which are key to functioning of the gut. Disruption of the intestinal barrier is associated with increased passage of luminal antigens into the mucosa, which further facilitates mucosal mast cell activation, inflammatory responses, and altered mast cell–enteric nerve interaction. Despite intensive research showing gut dysfunction to be associated with increased intestinal permeability and mucosal mast cell activation, the specific mechanisms linking mast cell activity with altered intestinal barrier in human disease remain unclear. This review describes the role played by mast cells in control of the intestinal mucosal barrier and their contribution to digestive diseases.

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