Particulate matter air pollution from the city of Quito, Ecuador, activates inflammatory signaling pathways <i>in vitro</i>

Cevallos, Victoria M; Díaz, Valeria; Sirois, Cherilyn M.

doi:10.1177/1753425917699864

Cited by 36 publications

(28 citation statements)

References 70 publications

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“…Nevertheless, to date, only the largest Ecuadorian cities (i.e., Quito, Guayaquil and Cuenca) have established permanent air quality monitoring stations. This follows a general trend throughout Ecuador, where only few studies have reported any effects of fine particulate matter or low air quality [13][14][15].…”

Section: Introductionmentioning

confidence: 81%

Lichens and Bromeliads as Bioindicators of Heavy Metal Deposition in Ecuador

et al. 2019

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We evaluated heavy metal deposition in Parmotrema arnoldii and Tillandsia usneoides in response to air pollution in Loja city, Ecuador. We assessed heavy metal (cadmium, copper, manganese, lead and zinc) content in these organisms at nine study sites inside Loja city and three control sites in nearby forests. Concentrations of all studied heavy metals (i.e., cadmium (Cd), copper (Cu), lead (Pb), manganese (Mn) and zinc (Zn)) were highest in downtown Loja. Our study confirms that passive monitoring using lichens and/or bromeliads can be an efficient tool to evaluate heavy metal deposition related to urbanization (e.g., vehicle emissions). We recommend these organisms to be used in cost-effective monitoring of air pollution in tropical countries.

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Section: Introductionmentioning

confidence: 81%

Lichens and Bromeliads as Bioindicators of Heavy Metal Deposition in Ecuador

et al. 2019

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“…Despite lots of work done, the mechanism that PM 2.5 aggravated CVDs was still not completely clear. More and more studies suggested that PM 2.5 may be an effective activator of the NLRP3 inflammasome in certain organs . A latest report showed that Al, Cr, Co, Ni, Se, Cd, Ba, Ti, and Pb in PM 2.5 could deposit in the prefrontal cortex of rats and regulate inflammation through NLRP3 inflammasome signal pathway .…”

Section: Discussionmentioning

confidence: 99%

“…More and more studies suggested that PM 2.5 may be an effective activator of the NLRP3 inflammasome in certain organs. 11,28,29 A latest report showed that Al, Cr, Co, Ni, Se, Cd, Ba, Ti, and Pb in PM 2.5 could deposit in the prefrontal cortex of rats and regulate inflammation through NLRP3 inflammasome signal pathway. 30 But in heart, only a report confirmed that IL-1β protein, the key downstream factor of NLRP3 inflammasome activation, played an important role in PM 2.5 -induced cardiac injury.…”

Section: Discussionmentioning

confidence: 99%

NLRP3 inflammasome activation is associated with PM_2.5‐induced cardiac functional and pathological injury in mice

Duan

Wang

Huang

et al. 2019

Environmental Toxicology

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Growing evidences indicate that inflammation induced by PM2.5 exposure has been considered as a major driving force for the development of cardiovascular diseases. However, the mechanisms underlying PM2.5‐induced cardiac injury remain unclear. This study aims to investigate the role of NLRP3 inflammasome in PM2.5‐induced cardiac functional and pathological injury in mice. In this study, BALB/c mice were intratracheally instilled with PM2.5 suspension (4.0 mg/kg BW) for 5 days to set up a cardiac injury model, which was evaluated by electrocardiogram monitoring, HE and Masson staining. Then, the effects of PM2.5 on the expression of α‐SMA, NLRP3, IL‐1β, and IL‐18 proteins and the activation of caspase‐1 and IL‐1β were investigated. The results showed that PM2.5 exposure induced characteristic abnormal ECG changes such as the abnormality of heart rhythm, tachycardia, and T‐wave reduction. Inflammatory cell infiltration and fibrosis were observed in the heart tissues of PM2.5‐exposed mice. Meanwhile, PM2.5 exposure increased the expression of α‐SMA. And, NLRP3 activation‐associated proteins of NLRP3, IL‐1β, IL‐18, Cleaved caspase‐1 p10, and Cleaved IL‐1β were upregulated in heart tissue of PM2.5‐induced mice. In summary, PM2.5 exposure could induce cardiac functional and pathological injury, which may be associated with the activation of NLRP3 inflammasome.

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“…38 The inflammasome. 41,42 Activation of NLRP3 results in further production of IL-1β, with consequent downstream effects driving the inflammatory process by signaling the production of IL-6 and hs-CRP. 39 The inflammatory cascade provoked by PM 2.5 is similar to the one instigated in metabolically unhealthy obese patients, in whom metabolically unhealthy adipose tissue is characterized by increased NLRP3 inflammasome activation.…”

Section: Residual CV Risk and Subclinical Inflammationmentioning

confidence: 99%

Cardiovascular Disease as a Result of the Interactions Between Obesity, Climate Change, and Inflammation: The COCCI Syndemic

Clearfield¹,

Davis²,

Weiss³

et al. 2018

Journal of Osteopathic Medicine

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Obesity and climate change conspire to create an environment in which subclinical vascular inflammation leads to progressive atherosclerosis, which contributes to the number 1 cause of global mortality: cardiovascular disease. The syndemic model requires 2 or more diseases or contributors to disease (such as obesity and climate change) clustering within a specific population in addition to the associated societal and social factors, ultimately creating an environment supportive of a greater adverse interaction. This article explores the syndemic of obesity and climate change as a driver for cardiovascular disease.

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Particulate matter air pollution from the city of Quito, Ecuador, activates inflammatory signaling pathways in vitro

Cited by 36 publications

References 70 publications

Lichens and Bromeliads as Bioindicators of Heavy Metal Deposition in Ecuador

Lichens and Bromeliads as Bioindicators of Heavy Metal Deposition in Ecuador

NLRP3 inflammasome activation is associated with PM_2.5‐induced cardiac functional and pathological injury in mice

Cardiovascular Disease as a Result of the Interactions Between Obesity, Climate Change, and Inflammation: The COCCI Syndemic

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Particulate matter air pollution from the city of Quito, Ecuador, activates inflammatory signaling pathways in vitro

Cited by 36 publications

References 70 publications

Lichens and Bromeliads as Bioindicators of Heavy Metal Deposition in Ecuador

Lichens and Bromeliads as Bioindicators of Heavy Metal Deposition in Ecuador

NLRP3 inflammasome activation is associated with PM2.5‐induced cardiac functional and pathological injury in mice

Cardiovascular Disease as a Result of the Interactions Between Obesity, Climate Change, and Inflammation: The COCCI Syndemic

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NLRP3 inflammasome activation is associated with PM_2.5‐induced cardiac functional and pathological injury in mice