Effects of collected road dusts on cell viability, inflammatory response, and oxidative stress in cultured human corneal epithelial cells

Yoon, Sunah; Han, Se-Hyun; Jeon, Ki-Jun; Kwon, Soonjo

doi:10.1016/j.toxlet.2017.12.012

Cited by 43 publications

(40 citation statements)

References 39 publications

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“…*A significant decrease relative to the control and 5 μg/ml #28, § A significant decrease compared to the control and 5 μg/ml #30, ¶ A significant difference between #28 and #30, **A significant difference compared with the control and all concentrations of #28 and #30, n = 8-10, LPS lipopolysaccharide. www.nature.com/scientificreports/ which is similar to the results of the current report 18,19 . The mechanisms underlying PM2.5-induced cell damage have been previously investigated.…”

Section: Discussionsupporting

confidence: 90%

“…The mechanisms underlying PM2.5-induced cell damage have been previously investigated. Yoon et al reported that the inflammatory response, mitochondrial activity, and oxidative stress participate in cell death 18 , and Gao et al found that reactive oxygen species and DNA damage result in corneal epithelial cell senescence following exposure to PM2.5 collected in Guangzhou 11,19 . Moreover, expression changes in cancer genes (oncogenes) are caused by PM2.5 exposure 12,20 .…”

Section: Discussionmentioning

confidence: 99%

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Effect and underlying mechanisms of airborne particulate matter 2.5 (PM2.5) on cultured human corneal epithelial cells

Kashiwagi

Ikoma

2020

Sci Rep

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Health problems caused by airborne particulate matter with a diameter less than 2.5 (PM2.5), especially in the respiratory system, have become a worldwide problem, but the influence and mechanisms of PM2.5 on the ocular surface have not been sufficiently elucidated. We investigated in vitro the onset and pathogenesis of corneal damage induced by PM2.5. Two types of PM2.5 samples originating from Beijing (designated #28) and the Gobi Desert (designated #30) were added to the culture medium of immortalized cultured human corneal epithelial cells (HCECs) to examine the effects on survival rates, autophagy, and proinflammatory cytokine production. Both types of PM2.5 significantly reduced the HCEC survival rate in a concentration-dependent manner by triggering autophagy. In particular, compared with #30, #28 induced much more severe damage in HCECs. Physical contact between PM2.5 and HCECs was not a primary contributor to PM2.5-induced HCEC damage. Among the 38 proinflammatory cytokines examined in this study, significant increases in the granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-6 levels and a significant reduction in the interleukin-8 level were detected in culture medium of PM2.5-exposed HCECs. Simultaneous addition of a GM-CSF inhibitor, suramin, alleviated the HCEC impairment induced by PM2.5. In conclusion, PM2.5 induces HCEC death by triggering autophagy. Some cytokines that are released from HCECs, including GM-CSF, may be involved in HCEC damage caused by PM2.5 exposure.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Effect and underlying mechanisms of airborne particulate matter 2.5 (PM2.5) on cultured human corneal epithelial cells

Kashiwagi

Ikoma

2020

Sci Rep

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“…These data are consistent with previous studies in primary two-dimensional HCET cultures, which also have shown that PM 2.5 treatment affected/decreased cell viability and increased levels of IL-1β. 40,41 FIGURE 8. Effects of PM 2.5 on inflammatory molecules in 3D HCET cultures.…”

Section: Discussionmentioning

confidence: 99%

Airborne Particulates Affect Corneal Homeostasis and Immunity

Somayajulu

Ekanayaka

McClellan

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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To determine the effects of airborne particulate matter (PM) <2.5 μm in vitro and on the normal and Pseudomonas aeruginosa (PA)-infected cornea. METHODS. An MTT viability assay tested the effects of PM 2.5 on mouse corneal epithelial cells (MCEC) and human corneal epithelial cells (HCET). MCEC were tested for reactive oxygen species using a 2 ,7-dichlorodihydrofluorescein assay; RT-PCR determined mRNA levels of inflammatory and oxidative stress markers in MCEC (HMGB1, toll-like receptor 2, IL-1β, CXCL2, GPX1, GPX2, GR1, superoxide dismutase 2, and heme oxygenase 1) and HCET (high mobility group box 1, CXCL2, and IL-1β). C57BL/6 mice also were infected and after 6 hours, the PM 2.5 was topically applied. Disease was graded by clinical score and evaluated by histology, plate count, myeloperoxidase assay, RT-PCR, ELISA, and Western blot. RESULTS. After PM 2.5 (25-200 μg/mL), 80% to 90% of MCEC and HCET were viable and PM exposure increased reactive oxygen species in MCEC and mRNA expression levels for inflammatory and oxidative stress markers in mouse and human cells. In vivo, the cornea of PA+PM 2.5 exposed mice exhibited earlier perforation over PA alone (confirmed histologically). In cornea, plate counts were increased after PA+PM 2.5 , whereas myeloperoxidase activity was significantly increased after PA+PM 2.5 over other groups. The mRNA levels for several proinflammatory and oxidative stress markers were increased in the cornea in the PA+PM 2.5 over other groups; protein levels were elevated for high mobility group box 1, but not toll-like receptor 4 or glutathione reductase 1. Uninfected corneas treated with PM 2.5 did not differ from normal. CONCLUSIONS. PM 2.5 triggers reactive oxygen species, upregulates mRNA levels of oxidative stress, inflammatory markers, and high mobility group box 1 protein, contributing to perforation in PA-infected corneas.

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“…UPM exerts numerous effects on cells and tissues [ 1 , 2 , 3 , 4 , 5 , 6 , 7 ]. It has been reported that exposure to UPM correlates with pulmonary dysfunction, cardiovascular disease, and hepatic fibrogenesis [ 28 , 29 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

“…Urban particulate matter (UPM) has become an increasing risk factor to human health particularly in urban areas. A number of studies have shown that UPM affects several organs; including the cardiovascular and pulmonary systems [ 1 , 2 , 3 , 4 ], as well as several cell types including lung cells; macrophages; and epithelial cells [ 5 , 6 , 7 ]. In addition; epidemiological studies have shown that UPM exposure is correlated with several human diseases including bronchial asthma, chronic obstructive pulmonary disease, lung cancer, atherosclerosis, ischemic stroke, congestive heart failure, myocardial ischemia, and birth defects [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Negative Cellular Effects of Urban Particulate Matter on Human Keratinocytes Are Mediated by P38 MAPK and NF-κB-dependent Expression of TRPV 1

Kwon

Park

Han³

et al. 2018

IJMS

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Urban particulate matter (UPM) exerts negative effects on various human organs. Transient receptor potential vanilloid 1 (TRPV1) is a polymodal sensory transducer that can be activated by multiple noxious stimuli. This study aimed to explore the effects of the UPM 1648a on the expression of TRPV1, and its regulatory mechanisms in HaCaT cells. UPM enhanced TRPV 1 promoter-luciferase reporter activity. UPM also increased expression of the TRPV 1 gene as evidenced by increased mRNA and protein levels of TRPV 1. In addition, elucidation of the underlying mechanism behind the UPM-mediated effects on TRPV 1 expression revealed that UPM can upregulate expression of the TRPV1 gene by activating activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB). The UPM treatment also altered Ca2+ influx and cell proliferation, as well as production of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). In addition, these UPM-induced effects were attenuated by SB203580 and ammonium pyrrolidinedithiocarbamate (PDTC). However, SP600125 and PD98059 did not alter the UPM-induced effects. Taken together, these findings indicate that UPM upregulates expression of the TRPV 1 gene, which is mediated by the p38 mitogen-activated protein kinase (MAPK) and NF-κB signaling pathways and suggest that UPM is a potential irritant that can induce skin processes such as aging and inflammatory responses.

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Effects of collected road dusts on cell viability, inflammatory response, and oxidative stress in cultured human corneal epithelial cells

Cited by 43 publications

References 39 publications

Effect and underlying mechanisms of airborne particulate matter 2.5 (PM2.5) on cultured human corneal epithelial cells

Effect and underlying mechanisms of airborne particulate matter 2.5 (PM2.5) on cultured human corneal epithelial cells

Airborne Particulates Affect Corneal Homeostasis and Immunity

Negative Cellular Effects of Urban Particulate Matter on Human Keratinocytes Are Mediated by P38 MAPK and NF-κB-dependent Expression of TRPV 1

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