Acute nitrogen dioxide (NO2) exposure enhances airway inflammation via modulating Th1/Th2 differentiation and activating JAK-STAT pathway

Ji, Xiaotong; Han, Ming; Yang, Yun; Li, Guangke; Sang, Nan

doi:10.1016/j.chemosphere.2014.10.039

Cited by 75 publications

(44 citation statements)

References 37 publications

(51 reference statements)

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“…However, toxicological studies conducted by Kastner et al [56] on cell cultures exposed to NO 2 at 0.08 ppm for four (04) days revealed a decrease in cell metabolism. In addition, exposure to diesel engine exhausts induces not only a severe inflammatory response in bronchoalveolar lavages characterized by allergen-specific Ig-E and Ig-G1 antibody production [57] but also a lymphocyte response with a cytokine profile type Th-2 (overproduction of Il-4) to the profile of Th-1 (IFN-gamma) during repeated exposure at 5 h / day for 7 days with 2.7 ppm NO 2 [58]. www.wjrr.org…”

Section: Discussionmentioning

confidence: 99%

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

Tito¹,

Messan²,

Togbenou³

et al. 2019

World Journal of Research and Review

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The inhalation of pollutants of automobile origin induces blood disturbances, especially noncommunicable diseases, in humans. However, there are no studies highlighting the effects induced by car pollutants. From this perspective, this study aims to evaluate the effects of at least two (02) pollutants, carbon monoxide (CO) and nitrogen dioxide (NO 2), on oxidative stress and inflammation after a single exposure for four hours (04 h). Materials and methods: Ten male Wistar strain rats were randomly divided into two groups of five (05): the control group (179.00 ± 5.916 g) unexposed and the group exposed to CO and NO 2 (188.00 ± 13.13 g). CO and NO 2 were produced by the combustion gas oil using a device contained in a sealed metal box supplied with ambient air by a pump. The ranges of CO and NO 2 concentrations to which the rats were exposed varied between 35 and 45 ppm and between 0.2 and 0.3 ppm, respectively. The blood samples were taken at 24 hours after the end of the manipulations. A malondialdehyde (MDA) assay was performed on supernatant using the GENESYS 10S UV Visible Spectrophotometer. Tumour Necrosis factor alpha (TNF-α) levels in the supernatant stored at-80 ° C were examined with an ELISA kit. Results: The mean values of MDA (17,771 ± 6.624 nM / ml) and TNF-α (83,050 ± 7.483 μg / ml) observed in the exposed group were significantly higher (p ˂ 0.01) than those recorded in the control group (MDA (7.097 ± 1.882 nM / ml) and TNF-α (6.410 ± 3.160 μg / ml). Conclusion: Exposure to CO and NO 2 for at least 4 hours induces the overproduction of reactive oxygen species (ROS) and the exacerbation of inflammation.

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Section: Discussionmentioning

confidence: 99%

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

Tito¹,

Messan²,

Togbenou³

et al. 2019

World Journal of Research and Review

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“…Mice deficient in STAT6 are completely protected from ovalbumin-induced goblet cell formation and mucus production (Kuperman et al, 1998). Other stimulus including nitrogen dioxide (Ji et al, 2015), secondhand cigarette smoke (Singh et al, 2011), and mycoplasma pneumonia (Hao et al, 2014) exposure also induce overexpression of airway mucins via the activation of STAT6 pathway in vivo. Signal transducer and activator of transcription 6 is phosphorylated by Janus kinases after stimulation by the cytokines IL-4 and interleukin 13 (IL-13) or PMA (Arinobu et al, 2000).…”

Section: The Flavonoid 74′-dihydroxyflavone Inhibits Muc5acmentioning

confidence: 99%

The Flavonoid 7,4′‐Dihydroxyflavone Inhibits MUC5AC Gene Expression, Production, and Secretion via Regulation of NF‐κB, STAT6, and HDAC2

Liu

Weir

Busse

et al. 2015

Phytotherapy Research

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Mucus overproduction is a significant component of the pathophysiology of obstructive lung diseases. Currently, there are only a few medications available that inhibit mucus production. Previous studies showed that glycyrrhizin, a triterpenoid in Glycyrrhiza uralensis (G. uralensis) inhibits mucin 5AC (MUC5AC) mRNA and protein expression. Other potential mucus production inhibitory compounds contained within in G. uralensis have not been fully investigated. The aim of the present study was to determine if the G. uralensis flavonoid 7,4'-dihydroxyflavone (7,4'-DHF), inhibits MUC5AC gene expression, mucus production and secretion and if so, to elucidate the mechanism of this inhibition. 7,4'-DHF significantly decreased phorbol 12-myristate 13-acetate (PMA) stimulated NCI-H292 human airway epithelial cell MUC5AC gene expression and mucus production, at a 28 fold lower concentration than glycyrrhizin (IC50 value of 1.4µM vs 38 µM, respectively), 7,4'-DHF also inhibited MUC5AC mucus secretion. Inhibition was associated with the suppression of NF-κB, STAT6 activation and enhanced HDAC2 expression. In a murine model of asthma, 7,4'-DHF treated mice exhibited a marked reduction in MUC5AC secretion in the bronchoalveolar lavage (BAL) fluid compared with control mice. These findings, together with previous findings linking NF-κB, STAT6 and HDAC2 modulation to the control of MUC5AC expression, demonstrate that 7,4'-DHF is a newly identified component of G. uralensis that regulates MUC5AC expression and secretion via regulation of NF-κB, STAT6 and HDAC2.

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“…15 The human health effects of exposure to SO 2 , NO 2 , O 3 and PM 10 have previously been reported. 7 16-19 Ozone, NO 2 and SO 2 pollutants can all cause lethal effects on the airway 20 such as an increase in bronchial reactivity, 21 22 airway oxidative stress, 23 pulmonary and systemic inflammation, 24 amplification of viral infections 25 and reduction in airway ciliary activity. 26 South Africa is one of the largest industrialised economies in the Southern Hemisphere and is the only industrialised regional energy producer on the African continent with significant mining and metallurgical activities.…”

Section: Introductionmentioning

confidence: 99%

Health risk of inhalation exposure to sub-10 µm particulate matter and gaseous pollutants in an urban-industrial area in South Africa: an ecological study

et al. 2017

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ObjectiveTo assess the health risks associated with exposure to particulate matter (PM10), sulphur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO) and ozone (O3).DesignThe study is an ecological study that used the year 2014 hourly ambient pollution data.SettingThe study was conducted in an industrial area located in Pretoria West, South Africa. The area accommodates a coal-fired power station, metallurgical industries such as a coke plant and a manganese smelter.Data and methodEstimate of possible health risks from exposure to airborne PM10, SO2, NO2, CO and O3 was performed using the US Environmental Protection Agency human health risk assessment framework. A scenario-assessment approach where normal (average exposure) and worst-case (continuous exposure) scenarios were developed for intermediate (24-hour) and chronic (annual) exposure periods for different exposure groups (infants, children, adults). The normal acute (1-hour) exposure to these pollutants was also determined.Outcome measuresPresence or absence of adverse health effects from exposure to airborne pollutants.ResultsAverage annual ambient concentration of PM10, NO2 and SO2 recorded was 48.3±43.4, 11.50±11.6 and 18.68±25.4 µg/m3, respectively, whereas the South African National Ambient Air Quality recommended 40, 40 and 50 µg/m3 for PM10, NO2 and SO2, respectively. Exposure to an hour's concentration of NO2, SO2, CO and O3, an 8-hour concentration of CO and O3, and a 24-hour concentration of PM10, NO2 and SO2 will not likely produce adverse effects to sensitive exposed groups. However, infants and children, rather than adults, are more likely to be affected. Moreover, for chronic annual exposure, PM10, NO2 and SO2 posed a health risk to sensitive individuals, with the severity of risk varying across exposed groups.ConclusionsLong-term chronic exposure to airborne PM10, NO2 and SO2 pollutants may result in health risks among the study population.

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Acute nitrogen dioxide (NO2) exposure enhances airway inflammation via modulating Th1/Th2 differentiation and activating JAK-STAT pathway

Cited by 75 publications

References 37 publications

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

The Flavonoid 7,4′‐Dihydroxyflavone Inhibits MUC5AC Gene Expression, Production, and Secretion via Regulation of NF‐κB, STAT6, and HDAC2

Health risk of inhalation exposure to sub-10 µm particulate matter and gaseous pollutants in an urban-industrial area in South Africa: an ecological study

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