Health Effects of Ambient Particulate Matter—Biological Mechanisms and Inflammatory Responses to In Vitro and In Vivo Particle Exposures

Abstract Purpose of Review A large body of epidemiological evidence demonstrates that exposure to particulate matter (PM) is associated with increased morbidity and mortality. Many epidemiology studies have investigated the health effects of PM in Europe and North America and focussed on traffic derived PM. However, elevated levels of PM are a global problem and the impacts of other sources of PM on health should be assessed. Biomass burning can increase PM levels in urban and rural indoor and outdoor environments in developed and developing countries. We aim to identify whether the health effects of traffic and biomass burning derived PM are similar by performing a narrative literature review. We focus on Thailand as haze episodes from agricultural biomass burning can substantially increase PM levels. Recent Findings Existing epidemiology, in vitro and in vivo studies suggest that biomass burning derived PM elicits toxicity via stimulation of oxidative stress, inflammation and genotoxicity. Thus, it is likely to cause similar adverse health outcomes to traffic PM, which causes toxicity via similar mechanisms. However, there is conflicting evidence regarding whether traffic or biomass burning derived PM is most hazardous. Also, there is evidence that PM released from different biomass sources varies in its toxic potency. Summary We recommend that epidemiology studies are performed in Thailand to better understand the impacts of PM emitted from specific biomass sources (e.g. agricultural burning). Further, experimental studies should assess the toxicity of PM emitted from more diverse biomass sources. This will fill knowledge gaps and inform evidence-based interventions that protect human health.

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In vivo and in vitro inflammatory responses to fine particulate matter (PM2.5) from China and California

Toxicology Letters ◽

10.1016/j.toxlet.2020.04.010 ◽

2020 ◽

Vol 328 ◽

pp. 52-60 ◽

Cited By ~ 1

Author(s):

Wanjun Yuan ◽

Ciara C. Fulgar ◽

Xiaolin Sun ◽

Christoph F.A. Vogel ◽

Ching-Wen Wu ◽

...

Keyword(s):

Particulate Matter ◽

Inflammatory Responses ◽

Fine Particulate Matter ◽

Fine Particulate

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

Combinatorial Chemistry & High Throughput Screening ◽

10.2174/1386207324666210412121226 ◽

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.

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Recent Advances in Particulate Matter and Nanoparticle Toxicology: A Review of theIn VivoandIn VitroStudies

BioMed Research International ◽

10.1155/2013/279371 ◽

2013 ◽

Vol 2013 ◽

pp. 1-22 ◽

Cited By ~ 127

Author(s):

Abderrahim Nemmar ◽

Jørn A. Holme ◽

Irma Rosas ◽

Per E. Schwarze ◽

Ernesto Alfaro-Moreno

Keyword(s):

Particulate Matter ◽

Health Effects ◽

Molecular Mechanisms ◽

Experimental Models ◽

Cellular Mechanisms ◽

Mortality And Morbidity ◽

Mechanisms Of Toxicity ◽

Adverse Health Effects

Epidemiological and clinical studies have linked exposure to particulate matter (PM) to adverse health effects, which may be registered as increased mortality and morbidity from various cardiopulmonary diseases. Despite the evidence relating PM to health effects, the physiological, cellular, and molecular mechanisms causing such effects are still not fully characterized. Two main approaches are used to elucidate the mechanisms of toxicity. One is the use ofin vivoexperimental models, where various effects of PM on respiratory, cardiovascular, and nervous systems can be evaluated. To more closely examine the molecular and cellular mechanisms behind the different physiological effects, the use of variousin vitromodels has proven to be valuable. In the present review, we discuss the current advances on the toxicology of particulate matter and nanoparticles based on these techniques.

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Carbon Monoxide-Releasing Molecule-2 Ameliorates Particulate Matter-Induced Aorta Inflammation via Toll-Like Receptor/NADPH Oxidase/ROS/NF-κB/IL-6 Inhibition

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/2855042 ◽

2021 ◽

Vol 2021 ◽

pp. 1-22

Author(s):

Thi Thuy Tien Vo ◽

Chien-Yi Hsu ◽

Yinshen Wee ◽

Yuh-Lien Chen ◽

Hsin-Chung Cheng ◽

...

Keyword(s):

Carbon Monoxide ◽

Particulate Matter ◽

Nadph Oxidase ◽

Adhesion Molecule ◽

Inflammatory Responses ◽

Air Pollutant ◽

Matrix Metalloproteinase 2 ◽

Beneficial Effects

Particulate matter (PM), a major air pollutant, may be associated with adverse cardiovascular effects. Reactive oxygen species- (ROS-) dependent proinflammatory cytokine production, such as interleukin-6 (IL-6), is a possible underlying mechanism. Carbon monoxide- (CO-) releasing molecule-2 (CORM-2) which liberates exogenous CO can exert many beneficial effects, particularly anti-inflammation and antioxidant effects. The purpose of this study was to explore the protective effects and underpinning mechanisms of CORM-2 on PM-induced aorta inflammation. Here, human aortic vascular smooth muscle cells (HASMCs) were utilized as in vitro models for the assessment of signaling pathways behind CORM-2 activities against PM-induced inflammatory responses, including Toll-like receptors (TLRs), NADPH oxidase, ROS, nuclear factor-kappa B (NF-κB), and IL-6. The modulation of monocyte adherence and HASMC migration, that are two critical cellular events of inflammatory process, along with their regulators, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and matrix metalloproteinase-2 (MMP-2) and MMP-9, in response to PM by CORM-2, were further evaluated. Finally, mice experiments under different conditions were conducted for the in vivo evaluation of CORM-2 benefits on the expression of inflammatory molecules including IL-6, ICAM-1, VCAM-1, MMP-2, and MMP-9. Our results found that PM could induce aorta inflammation in vitro and in vivo, as evidenced by the increase of IL-6 expression that was regulated by the TLR2 and TLR4/NADPH oxidase/ROS/NF-κB signaling pathway, thereby promoting ICAM-1- and VCAM-1-dependent monocyte adhesion and MMP-2- and MMP-9-dependent HASMC migration. Importantly, our experimental models demonstrated that CORM-2-liberated CO effectively inhibited the whole identified PM-induced inflammatory cascade in HASMCs and tissues. In conclusion, CORM-2 treatment may elicit multiple beneficial effects on inflammatory responses of aorta due to PM exposure, thereby providing therapeutic value in the context of inflammatory diseases of the cardiovascular system.

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Lipoproteins Are Responsible for the Pro-Inflammatory Property of Staphylococcus aureus Extracellular Vesicles

International Journal of Molecular Sciences ◽

10.3390/ijms22137099 ◽

2021 ◽

Vol 22 (13) ◽

pp. 7099

Author(s):

Pradeep Kumar Kopparapu ◽

Meghshree Deshmukh ◽

Zhicheng Hu ◽

Majd Mohammad ◽

Marco Maugeri ◽

...

Keyword(s):

Extracellular Vesicles ◽

Inflammatory Responses ◽

Surface Proteins ◽

Host Cells ◽

Immune Stimulation ◽

Domains Of Life ◽

Major Surface ◽

Staphylococcal Aureus

Staphylococcal aureus (S. aureus), a Gram-positive bacteria, is known to cause various infections. Extracellular vesicles (EVs) are a heterogeneous array of membranous structures secreted by cells from all three domains of life, i.e., eukaryotes, bacteria, and archaea. Bacterial EVs are implied to be involved in both bacteria–bacteria and bacteria–host interactions during infections. It is still unclear how S. aureus EVs interact with host cells and induce inflammatory responses. In this study, EVs were isolated from S. aureus and mutant strains deficient in either prelipoprotein lipidation (Δlgt) or major surface proteins (ΔsrtAB). Their immunostimulatory capacities were assessed both in vitro and in vivo. We found that S. aureus EVs induced pro-inflammatory responses both in vitro and in vivo. However, this activity was dependent on lipidated lipoproteins (Lpp), since EVs isolated from the Δlgt showed no stimulation. On the other hand, EVs isolated from the ΔsrtAB mutant showed full immune stimulation, indicating the cell wall anchoring of surface proteins did not play a role in immune stimulation. The immune stimulation of S. aureus EVs was mediated mainly by monocytes/macrophages and was TLR2 dependent. In this study, we demonstrated that not only free Lpp but also EV-imbedded Lpp had high pro-inflammatory activity.

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Involvement of HECTD1 in LPS-induced astrocyte activation via σ-1R-JNK/p38-FOXJ2 axis

Cell & Bioscience ◽

10.1186/s13578-021-00572-x ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Ying Tang ◽

Mengchun Zhou ◽

Rongrong Huang ◽

Ling Shen ◽

Li Yang ◽

...

Keyword(s):

Inflammatory Responses ◽

Astrocyte Activation ◽

Hect Domain ◽

P38 Inhibitor ◽

Ubiquitin Protein Ligase ◽

Primary Mouse ◽

Lps Treatment

Abstract Background Astrocytes participate in innate inflammatory responses within the mammalian central nervous system (CNS). HECT domain E3 ubiquitin protein ligase 1 (HECTD1) functions during microglial activation, suggesting a connection with neuroinflammation. However, the potential role of HECTD1 in astrocytes remains largely unknown. Results Here, we demonstrated that HECTD1 was upregulated in primary mouse astrocytes after 100 ng/ml lipopolysaccharide (LPS) treatment. Genetic knockdown of HECTD1 in vitro or astrocyte-specific knockdown of HECTD1 in vivo suppressed LPS-induced astrocyte activation, whereas overexpression of HECTD1 in vitro facilitated LPS-induced astrocyte activation. Mechanistically, we established that LPS activated σ-1R-JNK/p38 pathway, and σ-1R antagonist BD1047, JNK inhibitor SP600125, or p38 inhibitor SB203580 reversed LPS-induced expression of HECTD1, thus restored LPS-induced astrocyte activation. In addition, FOXJ2 functioned as a transcription factor of HECTD1, and pretreatment of primary mouse astrocytes with BD1047, SB203580, and SP600125 significantly inhibited LPS-mediated translocation of FOXJ2 into the nucleus. Conclusions Overall, our present findings suggest that HECTD1 participates in LPS-induced astrocyte activation by activation of σ-1R-JNK/p38-FOXJ2 pathway and provide a potential therapeutic strategy for neuroinflammation induced by LPS or any other neuroinflammatory disorders.

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Effects of ambient particulate matter on a reconstructed human corneal epithelium model

Scientific Reports ◽

10.1038/s41598-021-82971-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Ryota Ko ◽

Masahiko Hayashi ◽

Miho Tanaka ◽

Tomoaki Okuda ◽

Chiharu Nishita-Hara ◽

...

Keyword(s):

Particulate Matter ◽

Cell Viability ◽

Corneal Epithelium ◽

Dependent Manner ◽

Ambient Particulate Matter ◽

Tissue Sections ◽

Human Corneal Epithelium ◽

Vitro Model ◽

Dose Dependent

AbstractWe evaluated the effects of ambient particulate matter (PM) on the corneal epithelium using a reconstructed human corneal epithelium (HCE) model. We collected two PM size fractions [aerodynamic diameter smaller than 2.4 µm: PM0.3–2.4 and larger than 2.4 µm: PM>2.4] and exposed these tissues to PM concentrations of 1, 10, and 100 µg/mL for 24 h. After exposure, cell viability and interleukin (IL) IL-6 and IL-8 levels were determined, and haematoxylin and eosin and immunofluorescence staining of the zonula occludens-1 (ZO-1) were performed on tissue sections. In addition, the effects of a certified reference material of urban aerosols (UA; 100 µg/mL) were also examined as a reference. The viability of cells exposed to 100 μg/mL UA and PM>2.4 decreased to 76.2% ± 7.4 and 75.4% ± 16.1, respectively, whereas PM0.3–2.4 exposure had a limited effect on cell viability. These particles did not increase IL-6 and IL-8 levels significantly even though cell viability was decreased in 100 μg/mL UA and PM>2.4. ZO-1 expression was reduced in a dose-dependent manner in all groups. Reconstructed HCE could be used as an in vitro model to study the effects of environmental PM exposure on ocular surface cell viability and inflammation.

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Nociceptive Sensitization by Activation of Protease-Activated Receptor 2 in a Rat Model of Incisional Pain

Brain Sciences ◽

10.3390/brainsci11020144 ◽

2021 ◽

Vol 11 (2) ◽

pp. 144

Author(s):

Kanta Kido ◽

Norika Katagiri ◽

Hiromasa Kawana ◽

Shigekazu Sugino ◽

Masanori Yamauchi ◽

...

Keyword(s):

Postoperative Pain ◽

Inflammatory Responses ◽

Early Period ◽

Intraplantar Injection ◽

C Fibers ◽

Nociceptive Responses ◽

Incisional Pain ◽

Protease Activated Receptor 2

Postoperative pain and consequent inflammatory responses after tissue incision adversely affects many surgical patients due to complicated mechanisms. In this study, we examined whether activation of protease-activated receptor 2 (PAR-2), which is stimulated by tryptase from mast cells, elicits nociception and whether the PAR-2 antagonist could reduce incisional nociceptive responses in vivo and in vitro. The effects of a selective PAR-2 antagonist, N3-methylbutyryl-N-6-aminohexanoyl-piperazine (ENMD-1068), pretreatment on pain behaviors were assessed after plantar incision in rats. The effects of a PAR-2 agonist, SLIGRL-NH2, on nociception was assessed after the injection into the hind paw. Furthermore, the responses of C-mechanosensitive nociceptors to the PAR-2 agonist were observed using an in vitro skin–nerve preparation as well. Intraplantar injection of SLIGRL-NH2 elicited spontaneous nociceptive behavior and hyperalgesia. Local administration of ENMD-1068 suppressed guarding behaviors, mechanical and heat hyperalgesia only within the first few hours after incision. SLIGRL-NH2 caused ongoing activity in 47% of C-mechanonociceptors in vitro. This study suggests that PAR-2 may support early nociception after incision by direct or indirect sensitization of C-fibers in rats. Moreover, PAR-2 may play a regulatory role in the early period of postoperative pain together with other co-factors to that contribute to postoperative pain.

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Fucoxanthin-rich fraction from Sargassum fusiformis alleviates particulate matter-induced inflammation in vitro and in vivo

Toxicology Reports ◽

10.1016/j.toxrep.2021.02.005 ◽

2021 ◽

Vol 8 ◽

pp. 349-358

Author(s):

Yu-Lin Dai ◽

Yun-Fei Jiang ◽

Yu-An Lu ◽

Jiang-Bo Yu ◽

Min-Cheol Kang ◽

...

Keyword(s):

Particulate Matter

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