Chemical and microbial components of urban air PM cause seasonal variation of toxicological activity

Jalava, Pasi; Happo, Mikko S.; Huttunen, Kati; Sillanpää, Markus; Hillamo, Risto; Salonen, Raimo O.; Hirvonen, Maija-Riitta

doi:10.1016/j.etap.2015.06.023

Cited by 52 publications

(41 citation statements)

References 51 publications

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“…Urban PM 2.5 is a complicated mixture containing different chemical and microbial components, originating from different sources, and a major determinant of adverse health effects on the public . In this study, chemical analysis of PM 2.5 samples revealed abundant metals such as Al, Zn, Fe, as well as PAHs.…”

Section: Discussionmentioning

confidence: 72%

Association of EGF Receptor and NLRs signaling with Cardiac Inflammation and Fibrosis in Mice Exposed to Fine Particulate Matter

Jin

Wang

et al. 2016

J Biochem Mol Toxicol

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ЄAmbient fine particulate matter (PM2.5 ) could induce cardiovascular diseases (CVD), but the mechanism remains unknown. To investigate the roles of epidermal growth factor receptor (EGFR) and NOD-like receptors (NLRs) in PM2.5 -induced cardiac injury, we set up a BALB/c mice model of PM2.5 -induced cardiac inflammation and fibrosis with intratracheal instillation of PM2.5 suspension (4.0 mg/kg b.w.) for 5 consecutive days (once per day). After exposure, we found that mRNA levels of CXCL1, interleukin (IL)-6, and IL-18 were elevated, but interestingly, mRNA level of NLRP12 was significant decreased in heart tissue from PM2.5 -induced mice compared with those of saline-treated mice using real-time PCR. Protein levels of phospho-EGFR (Tyr1068), phospho-Akt (Thr308), NLRP3, NF-κB-p52/p100, and NF-κB-p65 in heart tissue of PM2.5 -exposed mice were all significantly increased using immunohistochemistry or Western blotting. Therefore, PM2.5 exposure could induce cardiac inflammatory injury in mice, which may be involved with EGFR/Akt signaling, NLRP3, and NLRP12.

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Section: Discussionmentioning

confidence: 72%

Association of EGF Receptor and NLRs signaling with Cardiac Inflammation and Fibrosis in Mice Exposed to Fine Particulate Matter

Jin

Wang

et al. 2016

J Biochem Mol Toxicol

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“…However, the underlying mechanisms of PM 2.5 -induced adverse cardiovascular effects have not been well understood. Ambient PM 2.5 is a complex mixture of different chemical and microbial components, originating from different sources, which is suggested to be a major determinant of the adverse health effects (Jalava et al, 2015). In the present study, there are three options of cutter bars on the high-volume air sampler, which are the total suspended particulates (TSP), PM 10 and PM 2.5 .…”

Section: Discussionmentioning

confidence: 95%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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-Epidemiological studies have confirmed that ambient fine particulate matter (PM 2.5 ) exposure is associated with cardiovascular disease (CVD). However, the underlying mechanisms in PM 2.5 exposure-induced heart injury are largely unknown. It has been acknowledged that NADPH oxidase (Nox) 4 plays a critical role in CVD development. To investigate the acute effects of PM 2.5 on the mouse heart and the role of Nox4 in PM 2.5 exposure-induced cardiac injury, C57BL/6J mice were instilled with saline or 1.5, 3.0, 6.0 mg/kg BW PM 2.5 suspension for two weeks (five days per week). The levels of malondialdehyde (MDA), super oxide dismutase (SOD), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β in heart supernatants were determined using related kits. The expression of Nox4, p67 phox , p47 phox and p22 phox in heart tissue was evaluated by immunofluorescence staining or Western blotting, respectively. Protein levels of p53, Bax, Bcl-2 and Caspase-3 in the heart were examined using immunohistochemical staining and Western blotting. TUNEL assay was used to measure myocardial apoptosis. PM 2.5 exposure leads to obvious cardiac injury. PM 2.5 exposure increases MDA level and iNOS activity, and decreases activity of SOD in heart supernatants of mice. High levels of TNF-α and IL-1β in heart supernatants of mice with PM 2.5 instillation were determined. Nox4 and Noxassociated subunits such as p67 phox , p47 phox and p22 phox expression levels were increased in heart tissue of mice after PM 2.5 exposure. Additionally, PM 2.5 exposure causes myocardial apoptosis in the mouse heart. This study suggested that Nox4 is involved in PM 2.5 exposure-induced cardiac injury in mice.

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“…Urban PM 2.5 is a complex mixture of different chemical and microbial components, originating from different sources, which is a major determinant of the adverse health effects (Jalava et al, ). In our study, the chemical and physical properties of PM 2.5 samples were analyzed, which revealed abundant metal elements, such as Al, Zn, Fe, and PAHs.…”

Section: Discussionmentioning

confidence: 99%

Involvement of EGF receptor signaling and NLRP12 inflammasome in fine particulate matter‐induced lung inflammation in mice

Jin

Zhang

et al. 2016

Environmental Toxicology

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Epidemiological studies have shown that exposure to ambient fine particulate matter (PM ) is associated with respiratory diseases. Lung inflammation is a central feature of many pulmonary diseases, which can be induced by PM exposure. However, the mechanisms underlying PM -induced lung inflammation remain unclear. To characterize the role of epidermal growth factor receptor (EGFR) and inflammasome in PM -induced lung inflammation in mice, 30 BALB/c mice were intrabroncheally instilled with saline and PM suspension (4.0 mg/kg b.w.) for 5 consecutive days, respectively. Bronchoalveolar lavage (BAL) was conducted and BAL fluid (BALF) was collected. The levels of reactive oxygen species (ROS), inducible nitric oxide synthase (iNOS), epidermal growth factor (EGF), CXCL1, interleukin (IL)-1β, and IL-18 in BALF were determined using ELISA. mRNA levels of IL-6, IL-1β, IL-18, CXCL1, IL-10, NLRP3, Caspase-1, and NLRP12 in lung tissues were determined by RT-PCR. Phospho-EGFR (Tyr1068) and phospho-Akt (Thr308) in lung tissues were examined using immunohistochemical staining and Western blotting, respectively. Protein levels of Caspase-1, NLRP3, NF-κB-p52/p100, and NF-κB-p65 in bronchial epithelium were examined using immunohistochemical staining. It was shown that PM exposure induced lung inflammation. Levels of total protein, ROS, iNOS, EGF, and CXCL1 and cell number in the BALF of mice exposed to PM were markedly elevated relative to the control. mRNA levels of CXCL1, IL-1β, and IL-18 in lung tissues of PM -exposed mice were increased in comparison with the control. However, level of NLRP12 mRNA in lung tissues of PM -exposed mice was reduced. Phospho-EGFR (Tyr1068) and phospho-Akt (Thr308) levels in the lungs of PM -instilled mice were higher than those in the lungs of the control. The protein levels of NF-κB-p52/p100 and NF-κB-p65 in bronchial epithelium of PM -exposed mice were also increased compared with the control. This study suggests that EGF-EGFR-Akt-NF-κB signaling and NLRP12 inflammasome may be associated with PM -induced lung inflammation in mice. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1121-1134, 2017.

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Chemical and microbial components of urban air PM cause seasonal variation of toxicological activity

Cited by 52 publications

References 51 publications

Association of EGF Receptor and NLRs signaling with Cardiac Inflammation and Fibrosis in Mice Exposed to Fine Particulate Matter

Association of EGF Receptor and NLRs signaling with Cardiac Inflammation and Fibrosis in Mice Exposed to Fine Particulate Matter

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Involvement of EGF receptor signaling and NLRP12 inflammasome in fine particulate matter‐induced lung inflammation in mice

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