Ambient fine particulate matter induces inflammatory responses of vascular endothelial cells through activating TLR-mediated pathway

Le, Yifei; Hu, Xiao; Zhu, Jing; Wang, Cui; Yang, Zhen; Lu, Dezhao

doi:10.1177/0748233719871778

Cited by 25 publications

(16 citation statements)

References 39 publications

(41 reference statements)

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“…Further studies revealed that PM 2.5 activates the NF‐κB pathway through Toll‐like receptors (TLRs) on the surface of lung macrophages, such as TLR2 or TLR4, which upregulate the release of inflammatory cytokines (Prueitt, Cohen, & Goodman, 2015; Van et al, 2001). PM 2.5 can also be identified by TLRs and has also been verified in HUVECs (Le et al, 2019). Besides, PM 2.5 ‐mediated ROS can also indirectly induce inflammation.…”

Section: Underlying Mechanisms Of Pm25‐induced Asmentioning

confidence: 84%

Progress in research on effect of PM_2.5 on occurrence and development of atherosclerosis

Tian

Zhao

et al. 2020

J of Applied Toxicology

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Fine particulate matter ≤2.5 μm (PM2.5) air pollution is regarded as one of the prominent risk factors that contributes to morbidity and mortality globally, among which cardiovascular disease (CVD) has been strongly associated with PM2.5 exposure and is a leading cause of death. Atherosclerosis (AS), the common pathological basis of many CVDs, is a progressive syndrome characterized by the accumulation of lipids and fibrous plaque in the arteries. Recent epidemiological and toxicological studies suggest that PM2.5 may also contribute to the development of AS, even at levels below the current air quality standards. In this paper, the complete pathological process of atherosclerotic plaque from occurrence to rupture leading to CVD was elaborated. Then, the growing epidemiological evidence linking PM2.5 to AS in humans was reviewed and summarized. Furthermore, the potential mechanisms of PM2.5‐mediated AS were discussed, including oxidative stress, inflammation, endothelial dysfunction, abnormal lipid metabolism, disturbance of the autonomic nervous system, and abnormal coagulation function. This paper aimed to provide a comprehensive view of the effect of PM2.5 on the occurrence and development of AS for better prevention and mitigation of adverse health impacts due to PM2.5 air pollution.

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Section: Underlying Mechanisms Of Pm25‐induced Asmentioning

confidence: 84%

Progress in research on effect of PM_2.5 on occurrence and development of atherosclerosis

Tian

Zhao

et al. 2020

J of Applied Toxicology

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“…TLR4/NADPH oxidase-dependent mechanisms are presumed to be involved (Kampfrath et al, 2011 ; Woodward et al, 2017 ). Activation of TLR2/NF-kB has also been demonstrated, both in vascular endothelial cells (Le et al, 2019 ) and in neuronal cells (Tian et al, 2021 ). In general, the TLR signaling activation results in the production of inflammatory cytokines and interferons (type 1) that occurs through a MyD88-dependent and interleukin-1 receptor (TRIF)-dependent pathways.…”

Section: Routes Of Pm Entering and Affecting The Brainmentioning

confidence: 97%

The Air We Breathe: Air Pollution as a Prevalent Proinflammatory Stimulus Contributing to Neurodegeneration

Jankowska-Kieltyka

Román

Nalepa

2021

Front. Cell. Neurosci.

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Air pollution is regarded as an important risk factor for many diseases that affect a large proportion of the human population. To date, accumulating reports have noted that particulate matter (PM) is closely associated with the course of cardiopulmonary disorders. As the incidence of Alzheimer’s disease (AD), Parkinson’s disease (PD), and autoimmune disorders have risen and as the world’s population is aging, there is an increasing interest in environmental health hazards, mainly air pollution, which has been slightly overlooked as one of many plausible detrimental stimuli contributing to neurodegenerative disease onset and progression. Epidemiological studies have indicated a noticeable association between exposure to PM and neurotoxicity, which has been gradually confirmed by in vivo and in vitro studies. After entering the body directly through the olfactory epithelium or indirectly by passing through the respiratory system into the circulatory system, air pollutants are subsequently able to reach the brain. Among the potential mechanisms underlying particle-induced detrimental effects in the periphery and the central nervous system (CNS), increased oxidative stress, inflammation, mitochondrial dysfunction, microglial activation, disturbance of protein homeostasis, and ultimately, neuronal death are often postulated and concomitantly coincide with the main pathomechanisms of neurodegenerative processes. Other complementary mechanisms by which PM could mediate neurotoxicity and contribute to neurodegeneration remain unconfirmed. Furthermore, the question of how strong and proven air pollutants are as substantial adverse factors for neurodegenerative disease etiologies remains unsolved. This review highlights research advances regarding the issue of PM with an emphasis on neurodegeneration markers, symptoms, and mechanisms by which air pollutants could mediate damage in the CNS. Poor air quality and insufficient knowledge regarding its toxicity justify conducting scientific investigations to understand the biological impact of PM in the context of various types of neurodegeneration.

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“…A previous study reported that PM2.5 increased the expression of TLR2 and TLR4 and promoted the secretion of inflammatory factors IL‐1β and IL‐6 in the aorta of mice as well as in the HUVECs. On the other hand, the suppression of TLR2 or TLR4 reduced the secretion of IL‐1β and IL‐6 (Le et al, 2019), suggesting that both TLR2 and TLR4 were involved in vascular inflammatory responses induced by PM2.5. Based on the above studies, PM2.5 triggers inflammation of VECs and then induces VECs activation via inflammatory signal pathway such as ERK/AKT/NF‐κB and COX‐2/mPGES‐1/PGE2.…”

Section: Pathophysiological Mechanisms Of Pm25‐induced Damage Of Vecsmentioning

confidence: 99%

The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

Xie

You

Zhi

et al. 2021

J of Applied Toxicology

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Several epidemiologic and toxicological studies have widely regarded ambient fine particulate matter (PM2.5), the particles with an aerodynamic diameter less than 2.5 μm, as a strong potential threat to human health. PM2.5 exposure is mainly through the respiratory tract where it can permeate the lung alveoli and enter the blood circulation. After going into the circulation, PM2.5 directly confronts the vascular endothelial cells (VECs). The VECs, which are lined up in the innermost layer of the blood vessels, are essential in the homeostasis of physiological processes. Thus, the damage and dysfunction of VECs is a common cause of various diseases. In this review, we summarize the toxicity of PM2.5 to VECs including the pathophysiological mechanism and the effects of VEC‐mediated physiological functions. The review has discussed the association of impaired VEC function by PM2.5 with various diseases, indicating that the VECs may be an effective assessment of public health recommendations under PM2.5 exposure. Therefore, reducing the adverse effect of PM2.5 on VECs will prevent the potential occurrence and fatality of the relevant diseases in the future.

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Ambient fine particulate matter induces inflammatory responses of vascular endothelial cells through activating TLR-mediated pathway

Cited by 25 publications

References 39 publications

Progress in research on effect of PM_2.5 on occurrence and development of atherosclerosis

Progress in research on effect of PM_2.5 on occurrence and development of atherosclerosis

The Air We Breathe: Air Pollution as a Prevalent Proinflammatory Stimulus Contributing to Neurodegeneration

The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

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Ambient fine particulate matter induces inflammatory responses of vascular endothelial cells through activating TLR-mediated pathway

Cited by 25 publications

References 39 publications

Progress in research on effect of PM2.5 on occurrence and development of atherosclerosis

Progress in research on effect of PM2.5 on occurrence and development of atherosclerosis

The Air We Breathe: Air Pollution as a Prevalent Proinflammatory Stimulus Contributing to Neurodegeneration

The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

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Product

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Progress in research on effect of PM_2.5 on occurrence and development of atherosclerosis

Progress in research on effect of PM_2.5 on occurrence and development of atherosclerosis