Acute changes in a respiratory inflammation marker in guards following Beijing air pollution controls

Shang, Jing; Khuzestani, Reza Bashiri; Huang, Wei; An, Jian-Xiong; Schauer, James J.; Fang, Daqing; Cai, Tianqi; Tian, Jingyu; Yang, Shujian; Guo, Bo; Zhang, Yuanxun

doi:10.1016/j.scitotenv.2017.12.109

Cited by 20 publications

(6 citation statements)

References 60 publications

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“…Previous studies have confirmed that PM2.5 exposure could cause acute airway inflammation 15,16 . In the present study, we explore the effect of PM2.5 on pulmonary inflammation in vivo.…”

Section: Resultsmentioning

confidence: 82%

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Jia

Liu

Guo

et al. 2020

Environmental Toxicology

106

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Particulate matter 2.5 (PM2.5)‐induced pulmonary inflammation has become a public concern in recent years. In which, the activation of the NLRP3/caspase‐1 pathway was closely related to the inflammatory response of various diseases. However, the promotion effect of the NLRP3/caspase‐1 pathway on PM2.5‐induced pulmonary inflammation remains largely unclear. Here, our data showed that PM2.5 exposure caused lung injury in the mice by which inflammatory cell infiltration occurred in lung and alveolar structure disorder. Meanwhile, the exposure of human bronchial epithelial cells (16HBE) to PM2.5 resulted in suppressed cell viability, as well as elevated cell apoptosis. Moreover, a higher level of inflammatory cytokine and activation of the NLRP3/caspase‐1 pathway in PM2.5‐induced inflammation mice models and 16HBE cells. Mechanistically, pretreatment with MCC950, a NLRP3/caspase‐1 pathway inhibitor, prevented PM2.5‐induced lung injury, inflammatory response, and the number of inflammatory cells in BALFs, as well as promoted cell viability and decreased inflammatory cytokine secretion. Collectively, our findings indicated that the NLRP3/caspase‐1 pathway serves a vital role in the pathological changes of pulmonary inflammation caused by PM2.5 exposure. MCC950 was expected to be the therapeutic target of PM2.5 inhalation mediated inflammatory diseases.

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“…Previous studies have confirmed that PM2.5 exposure could cause acute airway inflammation 15,16 . In the present study, we explore the effect of PM2.5 on pulmonary inflammation in vivo.…”

Section: Resultsmentioning

confidence: 82%

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Jia

Liu

Guo

et al. 2020

Environmental Toxicology

106

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“…This suggests that exhaled NO is unaffected by growth and development at high‐altitude, which is a common mode of adaptive response to high altitude hypoxia (Beall et al, ; Frisancho & Baker, ; Monge, ; Malik & Singh, ). Finally, differences in exhaled NO between males and females, and differences between the US reference group and the Quechua sea‐level groups, strongly suggest that much of the overall variance that we observed in exhaled NO has little to do with the adaptive response to hypobaric hypoxia, and perhaps more to do with unmeasured local environmental conditions, for example, pollution leading to lung inflammation (Dressel et al, ; Dweik et al, ; Shang et al, ), or population level characteristics that were not measured, for example, fitness‐level (Green, Maiorana, O'Driscoll, & Taylor, ; Jungersten, Ambring, Wall, & Wennmalm, ), diet (Iijima et al, ; Larsen, Ekblom, Sahlin, Lundberg, & Weitzberg, ) and so forth.…”

Section: Discussionmentioning

confidence: 83%

Exhaled nitric oxide in ethnically diverse high‐altitude native populations: A comparative study

Ghosh

Kiyamu

Contreras

et al. 2019

American J Phys Anthropol

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Objectives: Andean and Tibetan high-altitude natives exhibit a high concentration of nitric oxide (NO) in the lungs, suggesting that NO plays an adaptive role in offsetting hypobaric hypoxia. We examined the exhaled NO concentration as well as partial pressure of several additional high-altitude native populations in order to examine the possibility that this putative adaptive trait, that is, high exhaled NO, is universal. Methods: We recruited two geographically diverse highland native populations, Tawang Monpa (TM), a Tibetan derived population in North-Eastern India (n = 95, sampled at an altitude of~3,200 m), and Peruvian Quechua from the highland Andes (n = 412). The latter included three distinct subgroups defined as those residing at altitude (Q-HAR, n = 110, sampled at 4,338 m), those born and residing at sea-level (Q-BSL, n = 152), and those born at altitude but migrant to sea-level (Q-M, n = 150).In addition, we recruited a referent sample of lowland natives of European ancestry from Syracuse, New York. Fraction of exhaled NO concentrations were measured using a NIOX NIMO following the protocol of the manufacturer.Results: Partial pressure of exhaled nitric oxide (PENO) was significantly lower (p < .05) in both high-altitude resident groups (TM = 6.2 ± 0.5 nmHg and Q-HAR = 5.8 ± 0.5 nmHg), as compared to the groups measured at sea level (USA = 14.6 ± 0.7 nmHg, Q-BSL = 18.9 ± 1.6 nmHg, and Q-M = 19.2 ± 1.7 nmHg).PENO was not significantly different between TM and Q-HAR (p < .05).Conclusion: In contrast to previous work, we found lower PENO in populations at altitude (compared to sea-level) and no difference in PENO between Tibetan and Andean highland native populations. These results do not support the hypothesis that high nitric oxide in human lungs is a universal adaptive mechanism of highland native populations to offset hypobaric hypoxia. K E Y W O R D SAndean Quechua, exhaled nitric oxide, hypobaric hypoxia, Tawang Monpa

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“… 8 , 9 Increasing evidence supported that PM 2.5 exposure was closely associated with the increased risk of premature mortality from respiratory diseases. 10 , 11 , 12 , 13 One large-scale epidemiological study in China reported that each 10 μg/m 3 increase in 2-day moving average level of PM 2.5 was associated with 0.29% increment in respiratory mortality. 14 Moreover, a few recent studies used years of life lost (YLL), a complementary index of mortality count, to evaluate the disease burden caused by PM 2.5 exposure.…”

Section: Introductionmentioning

confidence: 99%

Changes in Life Expectancy of Respiratory Diseases from Attaining Daily PM2.5 Standard in China: A Nationwide Observational Study

Yang

Ruan

et al. 2020

The Innovation

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Acute changes in a respiratory inflammation marker in guards following Beijing air pollution controls

Cited by 20 publications

References 60 publications

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Exhaled nitric oxide in ethnically diverse high‐altitude native populations: A comparative study

Changes in Life Expectancy of Respiratory Diseases from Attaining Daily PM2.5 Standard in China: A Nationwide Observational Study

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