scholarly journals 3-Hydroxy-5,6-epoxy-β-ionone Isolated from Invasive Harmful Brown Seaweed Sargassum Horneri Protects MH-S Mouse Lung Cells from Urban Particulate Matter-Induced Inflammation

2021 ◽  
Vol 11 (22) ◽  
pp. 10929
Author(s):  
K. K. Asanka Sanjeewa ◽  
Hyun-Soo Kim ◽  
Hyo-Geun Lee ◽  
Thilina U. Jayawardena ◽  
D. P. Nagahawatta ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Air Pollution ◽  
Particulate Matter ◽  
Brown Seaweed ◽  
Dust Storms ◽  
Sargassum Horneri ◽  
Potential Candidate ◽  
Western Blots ◽  
Edible Seaweed ◽  
Anti Inflammatory

Air pollution is a process that mixes pollutants into the atmosphere, which is potentially harmful to humans and causes negative impacts on the surrounding environment (biotic and abiotic). The negative health effects associated with air pollution have been reported from both indoor and outdoor environments. Specifically, dust storms originating in Chinese and Mongolian desert areas introduce significant amounts of particulate matter (PM) to the Korean atmosphere. Previously, several studies reported that urban PM (UPM) is a potential agent that causes inflammation in the lungs by altering multiple signal transduction pathways; therefore, screening and identification of anti-inflammatory compounds against UPM-induced inflammation is an urgent requirement. In the present study, we attempted to study the anti-inflammatory properties of 3-Hydroxy-5,6-epoxy-β-ionone (HEBI), a pure compound isolated from invasive brown seaweed, Sargassum horneri (brown edible seaweed), against UPM-stimulated lung macrophages (MH-S). Anti-inflammatory parameters of HEBI were evaluated using Western blots, ELISA, RT-qPCR, and MTT assays. According to the results, HEBI at concentrations between 31.3 and 125 µg/mL reduced UPM-induced NO, PGE2, and pro-inflammatory cytokine production via blocking the downstream signal transduction of NF-κB and MAPKs. Specifically, HEBI down-regulated the mRNA expression levels of Toll-like receptors 2 and 4, which are well-known NF-κB and MAPKs stimulators. Taken together, HEBI is a potential candidate to develop functional foods and active ingredients in cosmeceuticals because of its profound effects against UPM-induced inflammation in MH-S macrophages.

scholarly journals Sargachromenol Isolated from Sargassum horneri Inhibits Particulate Matter-Induced Inflammation in Macrophages through Toll-like Receptor-Mediated Cell Signaling Pathways

Marine Drugs ◽  
2021 ◽  
Vol 20 (1) ◽  
pp. 28
Author(s):  
D. P. Nagahawatta ◽  
Hyun-Soo Kim ◽  
Young-Heun Jee ◽  
Thilina U. Jayawardena ◽  
Ginnae Ahn ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Brown Seaweed ◽  
Sargassum Horneri ◽  
Enzyme Linked Immunosorbent Assay ◽  
Potential Candidate ◽  
Toll Like Receptor ◽  
Natural Habitats ◽  
Western Blots ◽  
Potent Inducer ◽  
Anti Inflammatory

Sargassum horneri is an invasive brown seaweed that grows along the shallow coastal areas of the Korean peninsula, which are potentially harmful to fisheries and natural habitats in the areas where it is accumulated. Therefore, the author attempted to evaluate the anti-inflammatory mechanism of Sargachromenol isolated from S. horneri against particulate matter (PM)-stimulated RAW 264.7 macrophages. PM is a potent inducer of respiratory diseases such as lung dysfunctions and cancers. In the present study, the anti-inflammatory properties of Sargachromenol were validated using enzyme-linked immunosorbent assay (ELISA), Western blots, and RT-qPCR experiments. According to the results, Sargachromenol significantly downregulated the PM-induced proinflammatory cytokines, Prostaglandin E2 (PGE2), and Nitric Oxide (NO) secretion via blocking downstream activation of Toll-like receptor (TLR)-mediated nuclear factor kappa B (NF-κB) and MAPKs phosphorylation. Thus, Sargachromenol is a potential candidate for innovation in various fields including pharmaceuticals, cosmeceuticals, and functional food.

The protective effect of Sargassum horneri against particulate matter-induced inflammation in lung tissues of an in vivo mouse asthma model

2019 ◽  
Vol 10 (12) ◽  
pp. 7995-8004 ◽  
Author(s):  
K. K. Asanka Sanjeewa ◽  
Thilin U. Jayawardena ◽  
Hyo Geun Lee ◽  
Kalahe Hewage Iresha Nadeeka Madushani Herath ◽  
Youngheun Jee ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Protective Effect ◽  
Brown Seaweed ◽  
Sargassum Horneri ◽  
Asthma Model ◽  
Anti Inflammatory

Sargassum horneri is an edible brown seaweed with potential anti-inflammatory properties.

Sources of Air Pollution

2018 ◽  
pp. 220-258
Author(s):  
Abderrezak Khelfi
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Adverse Effects ◽  
Chemical Reactions ◽  
Dust Storms ◽  
Pollution Sources ◽  
Atmospheric Gases ◽  
Secondary Pollutants ◽  
Harmful Substances ◽  
Life On Earth

This chapter describes how air is a complex natural gaseous system essential to support life on Earth. Air pollution comes from a wide variety of sources, which discharge of harmful substances into the atmosphere, causing adverse effects to humans and the environment. They can be natural or anthropogenic. Natural air pollution sources are multiple and include volcanic eruption, fire, ocean vapors, dust storms and fermentation of organic materials. However, the range and quantities of chemicals discharged into the atmosphere from industry, transport, agriculture, energy production, domestic heating, and many other human activities, have increased dramatically. Some pollutants are emitted directly into the atmosphere and are known as primary pollutants (NOx, SOx, particulate matter, etc.). Others are formed in the air as a result of chemical reactions with other pollutants and atmospheric gases; these are known as secondary pollutants like ozone. This chapter provides an overview on air pollution sources as well as the ways in which pollutants can affect human health and the environment.

Nutraceuticals with anti-inflammatory and anti-oxidant properties as intervention for reducing the health effects of fine particulate matter: Potential and Prospects

2021 ◽  
Vol 24 ◽  
Author(s):  
Tanwi Trushna ◽  
Amit K. Tripathi ◽  
Sindhuprava Rana ◽  
Rajnarayan R. Tiwari
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Human Health ◽  
Health Effects ◽  
In Vivo Studies ◽  
Future Research ◽  
Individual Level ◽  
Anti Inflammatory

: Air pollution, especially particulate matter pollution adversely affects human health. A growing pool of evidence has emerged which underscores the potential of individual-level nutritional interventions in attenuating the adverse health impact of exposure to PM2.5. Although controlling emission and reducing the overall levels of air pollution remains the ultimate objective globally, the sustainable achievement of such a target and thus consequent protection of human health will require a substantial amount of time and concerted efforts worldwide. In the meantime, smaller-scale individual-level interventions that can counter the inflammatory or oxidative stress effects triggered by exposure to particulate matter may be utilized to ameliorate the health effects of PM2.5 pollution. One such intervention is incorporation of nutraceuticals in the diet. Here, we present a review of the evidence generated from various in vitro, in vivo and human studies regarding the effects of different anti-inflammatory and antioxidant nutraceuticals in ameliorating the health effects of particulate matter air pollution. The studies discussed in this review suggest that these nutraceuticals when consumed as a part of the diet, or as additional supplementation, can potentially negate the cellular level adverse effects of exposure to particulate pollution. The potential benefits of adopting a non-pharmacological diet-based approach to air pollution-induced disease management have also been discussed. We argue that before a nutraceuticals-based approach can be used for widespread public adoption, further research, especially human clinical trials, is essential to confirm the beneficial action of relevant nutraceuticals and to explore the safe limits of human supplementation and the risk of side effects. Future research should focus on systematically translating bench-based knowledge regarding nutraceuticals gained from in-vitro and in-vivo studies into clinically usable nutritional guidelines.

scholarly journals Astaxanthin Suppresses PM2.5-Induced Neuroinflammation by Regulating Akt Phosphorylation in BV-2 Microglial Cells

2020 ◽  
Vol 21 (19) ◽  
pp. 7227 ◽  
Author(s):  
Ryeong-Eun Kim ◽  
Chan Young Shin ◽  
Seol-Heui Han ◽  
Kyoung Ja Kwon
Keyword(s):  
Nitric Oxide ◽  
Air Pollution ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Microglial Cells ◽  
Akt Phosphorylation ◽  
Fine Particulate ◽  
Pm2.5 Exposure ◽  
Anti Inflammatory ◽  
The Brain

Air pollution has become one of the most serious issues for human health and has been shown to be particularly concerning for neural and cognitive health. Recent studies suggest that fine particulate matter of less than 2.5 (PM2.5), common in air pollution, can reach the brain, potentially resulting in the development and acceleration of various neurological disorders including Alzheimer’s disease, Parkinson’s disease, and other forms of dementia, but the underlying pathological mechanisms are not clear. Astaxanthin is a red-colored phytonutrient carotenoid that has been known for anti-inflammatory and neuroprotective effects. In this study, we demonstrated that exposure to PM2.5 increases the neuroinflammation, the expression of proinflammatory M1, and disease-associated microglia (DAM) signature markers in microglial cells, and that treatment with astaxanthin can prevent the neurotoxic effects of this exposure through anti-inflammatory properties. Diesel particulate matter (Sigma-Aldrich) was used as a fine particulate matter 2.5 in the present study. Cultured rat glial cells and BV-2 microglial cells were treated with various concentrations of PM2.5, and then the expression of various inflammatory mediators and signaling pathways were measured using qRT-PCR and Western blot. Astaxanthin was then added and assayed as above to evaluate its effects on microglial changes, inflammation, and toxicity induced by PM2.5. PM2.5 increased the production of nitric oxide and reactive oxygen species and upregulated the transcription of various proinflammatory markers including Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor α (TNFα), inducible nitric oxide synthase (iNOS), triggering receptor expressed on myeloid cells 2 (TREM2), Toll-like receptor 2/4 (TLR2/4), and cyclooxygenase-2 (COX-2) in BV-2 microglial cells. However, the mRNA expression of IL-10 and arginase-1 decreased following PM2.5 treatment. PM2.5 treatment increased c-Jun N-terminal kinases (JNK) phosphorylation and decreased Akt phosphorylation. Astaxanthin attenuated these PM2.5-induced responses, reducing transcription of the proinflammatory markers iNOS and heme oxygenase-1 (HO-1), which prevented neuronal cell death. Our results indicate that PM2.5 exposure reformulates microglia via proinflammatory M1 and DAM phenotype, leading to neurotoxicity, and the fact that astaxanthin treatment can prevent neurotoxicity by inhibiting transition to the proinflammatory M1 and DAM phenotypes. These results demonstrate that PM2.5 exposure can induce brain damage through the change of proinflammatory M1 and DAM signatures in the microglial cells, as well as the fact that astaxanthin can have a potential beneficial effect on PM2.5 exposure of the brain.

scholarly journals The effects of particulate matter air pollution on respiratory health and on the cardiovascular system

2012 ◽  
Vol 51 (3) ◽  
pp. 190-199 ◽  
Author(s):  
Zala Pražnikar ◽  
Jure Pražnikar
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Cardiovascular System ◽  
Respiratory Health ◽  
Volcanic Eruptions ◽  
Dust Storms ◽  
Size Fractions ◽  
Short Term Exposure ◽  
Increased Risk ◽  
Acute And Chronic Exposure

The effects of particulate matter air pollution on respiratory health and on the cardiovascular system Particulate matter (PM) is a major component of urban air pollution and has a significant effect on human health. Natural PM sources are volcanic eruptions, dust storms, forest and grassland fires, living vegetation and sea spray. Traffic, domestic heating, power plants and various industrial processes generate significant amounts of anthropogenic PM. PM consists of a complex mixture of solid and liquid particles of organic and inorganic substances suspended in the air. The chemical composition of particles is very complex and depends on emission sources, meteorological conditions and their aerodynamic diameter. Several epidemiological studies have demonstrated that exposure to PM of varying size fractions is associated with an increased risk of respiratory and cardiovascular diseases. Adverse health effects have been documented from studies of both acute and chronic exposure. The most severe effects in terms of overall health burden include a significant reduction in life expectancy by a several months for the average population, which is linked to long-term exposure to moderate concentrations of PM. Nevertheless, numerous deaths and serious cardiovascular and respiratory problems have also been attributed to short-term exposure to peak levels of PM. Although many studies attribute greater toxicity to smaller size fractions, which are able to penetrate deeper into the lung, the molecular mechanisms and the size fractions of the PM that are responsible for the observed diseases are not completely understood.

scholarly journals Association between African Dust Transport and Acute Exacerbations of COPD in Miami

2020 ◽  
Vol 9 (8) ◽  
pp. 2496
Author(s):  
Miguel Pardinas Gutierrez ◽  
Paquita Zuidema ◽  
Mehdi Mirsaeidi ◽  
Michael Campos ◽  
Naresh Kumar
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Ambient Temperature ◽  
Acute Exacerbation ◽  
Dust Storms ◽  
Saharan Dust ◽  
Dust Exposure ◽  
Chronic Obstructive ◽  
Copd Patients ◽  
Dust Events

Background: Air pollution is increasingly recognized as a risk factor for acute exacerbation of chronic obstructive pulmonary disease (COPD). Changing climate and weather patterns can modify the levels and types of air pollutants. For example, dust outbreaks increase particulate air pollution. Objective: This paper examines the effect of Saharan dust storms on the concentration of coarse particulate matter in Miami, and its association with the risk of acute exacerbation of COPD (AECOPD). Methods: In this prospective cohort study, 296 COPD patients (with 313 events) were followed between 2013 and 2016. We used Light Detection and Ranging (LIDAR) and satellite-based Aerosol Optical Depth (AOD) to identify dust events and quantify particulate matter (PM) exposure, respectively. Exacerbation events were modeled with respect to location- and time-lagged dust and PM exposures, using multivariate logistic regressions. Measurements and main results: Dust duration and intensity increased yearly during the study period. During dust events, AOD increased by 51% and particulate matter ≤2.5 µm in aerodynamic diameter (PM2.5) increased by 25%. Adjusting for confounders, ambient temperature and local PM2.5 exposure, one-day lagged dust exposure was associated with 4.9 times higher odds of two or more (2+ hereto after) AECOPD events (odds ratio = 4.9; 95% CI = 1.8–13.4; p < 0.001). Ambient temperature exposure also showed a significant association with 2+ and 3+ AECOPD events. The risk of AECOPD lasted up to 15 days after dust exposure, declining from 10× higher on day 0 to 20% higher on day 15. Conclusions: Saharan dust outbreaks observed in Miami elevate the concentration of PM and increase the risk of AECOPD in COPD patients with recurring exacerbations.

scholarly journals Endogenous itaconate is not required for particulate matter-induced NRF2 expression or inflammatory response

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Kaitlyn A Sun ◽  
Yan Li ◽  
Angelo Y Meliton ◽  
Parker S Woods ◽  
Lucas M Kimmig ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Inflammatory Response ◽  
Lung Inflammation ◽  
Mitochondrial Enzyme ◽  
Nrf2 Activation ◽  
Anti Inflammatory ◽  
Nrf2 Expression

Particulate matter (PM) air pollution causes cardiopulmonary mortality via macrophage-driven lung inflammation; however, the mechanisms are incompletely understood. RNA-sequencing demonstrated Acod1 (Aconitate decarboxylase 1) as one of the top genes induced by PM in macrophages. Acod1 encodes a mitochondrial enzyme that produces itaconate, which has been shown to exert anti-inflammatory effects via NRF2 after LPS. Here, we demonstrate that PM induces Acod1 and itaconate, which reduced mitochondrial respiration via complex II inhibition. Using Acod1-/- mice, we found that Acod1/endogenous itaconate does not affect PM-induced inflammation or NRF2 activation in macrophages in vitro or in vivo. In contrast, exogenous cell permeable itaconate, 4-octyl itaconate (OI) attenuated PM-induced inflammation in macrophages. OI was sufficient to activate NRF2 in macrophages; however, NRF2 was not required for the anti-inflammatory effects of OI. We conclude that the effects of itaconate production on inflammation are stimulus-dependent, and that there are important differences between endogenous and exogenously-applied itaconate.

scholarly journals Endogenous itaconate is not required for particulate matter-induced NRF2 expression or inflammatory response

2020 ◽  
Author(s):  
Kaitlyn A. Sun ◽  
Yan Li ◽  
Angelo Y. Meliton ◽  
Parker S. Woods ◽  
Lucas M. Kimmig ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Inflammatory Response ◽  
Rna Sequencing ◽  
Mitochondrial Respiration ◽  
Lung Inflammation ◽  
Mitochondrial Enzyme ◽  
Nrf2 Activation ◽  
Anti Inflammatory ◽  
Nrf2 Expression

ABSTRACTParticulate matter (PM) air pollution causing significant cardiopulmonary mortality via macrophage-driven lung inflammation; however, the mechanisms are not completely understood. RNA-sequencing demonstrated Acod1 (Aconitate decarboxylase 1) as one of the top genes induced by PM in macrophages. Acod1 encodes a mitochondrial enzyme that produces itaconate, which has been shown to exert anti-inflammatory effects via NRF2 after LPS. Here, we demonstrate that PM induces Acod1 and itaconate, which reduced mitochondrial respiration via complex II inhibition. Using Acod1-/- macrophages, we found that Acod1/endogenous itaconate was not required for PM-induced inflammation or NRF2 activation. In contrast to endogenous itaconate, exogenous cell permeable form of itaconate (4-octyl itaconate (OI)) attenuated the PM-induced inflammation and activated NRF2 but NRF2 was not required for the anti-inflammatory effects of OI. We conclude that the effects of itaconate production on inflammation are stimulus-dependent, and that there are important differences between endogenous and exogenously-applied itaconate.

Sign in / Sign up

Export Citation Format

Share Document