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

ABSTRACT: 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.

SUBMITTER: Kashiwagi K

PROVIDER: S-EPMC7659009 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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

Kashiwagi Kenji K Iizuka Yoko Y

Scientific reports 20201111 1

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 imm ...[more]

PMID: 33177636

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Project description:Background: In classrooms high concentrations of particulate matter PM10 were measured. It is unknown whether the hazard of indoor particles is similar to that of the better studied outdoor particles. This study therefore analyzed adverse biological effects of classroom in comparison to outdoor PM10. Methods: Samples were taken from six schools during teaching hours. Genome-wide gene expression in human bronchial BEAS-2B epithelial cells was analyzed, and regulated genes were verified by quantitative PCR. Polycyclic aromatic hydrocarbons (PAH), endotoxin, and cat allergen Fel d 1 were analyzed with standard methods. Enhancement of allergic reactivity by PM10 was confirmed with CD63 upregulation in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM10-exposed human peripheral blood monocytes. Results: Indoor PM10 induced SERPINB2 (involved in blood coagulation) and inflammatory genes (like CXCL6, CXCL1, IL6, IL8, all p<0.001). Outdoor PM10 induced xenobiotic metabolizing enzymes (CYP1A1, CYP1B1, TIPARP, all p<0.001). The induction of inflammatory genes by indoor PM10 could be explained by endotoxin (indoor 128.5±42.2EU/mg versus outdoor 13.4±21.5EU/mg, p<0.001), the induction of CYP by outdoor PAH (indoor 8.3±4.9ng/mg versus outdoor 16.7±15.2ng/mg, p<0.01). The induction of SERPINB2 was confirmed by a more rapid human blood coagulation (p<0.05). Indoor PM10 had no effect on the allergic reactivity from human primary basophils, except in cat allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM10 (p<0.001). Conclusions: Indoor PM10, compared to outdoor PM10, was 6 times higher, had a different composition, and on an equal weight basis induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM10 had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM10 seem reasonable, perhaps by intensified ventilation.

Project description:Background: In classrooms high concentrations of particulate matter PM10 were measured. It is unknown whether the hazard of indoor particles is similar to that of the better studied outdoor particles. This study therefore analyzed adverse biological effects of classroom in comparison to outdoor PM10. Methods: Samples were taken from six schools during teaching hours. Genome-wide gene expression in human bronchial BEAS-2B epithelial cells was analyzed, and regulated genes were verified by quantitative PCR. Polycyclic aromatic hydrocarbons (PAH), endotoxin, and cat allergen Fel d 1 were analyzed with standard methods. Enhancement of allergic reactivity by PM10 was confirmed with CD63 upregulation in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM10-exposed human peripheral blood monocytes. Results: Indoor PM10 induced SERPINB2 (involved in blood coagulation) and inflammatory genes (like CXCL6, CXCL1, IL6, IL8, all p<0.001). Outdoor PM10 induced xenobiotic metabolizing enzymes (CYP1A1, CYP1B1, TIPARP, all p<0.001). The induction of inflammatory genes by indoor PM10 could be explained by endotoxin (indoor 128.5M-BM-142.2EU/mg versus outdoor 13.4M-BM-121.5EU/mg, p<0.001), the induction of CYP by outdoor PAH (indoor 8.3M-BM-14.9ng/mg versus outdoor 16.7M-BM-115.2ng/mg, p<0.01). The induction of SERPINB2 was confirmed by a more rapid human blood coagulation (p<0.05). Indoor PM10 had no effect on the allergic reactivity from human primary basophils, except in cat allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM10 (p<0.001). Conclusions: Indoor PM10, compared to outdoor PM10, was 6 times higher, had a different composition, and on an equal weight basis induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM10 had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM10 seem reasonable, perhaps by intensified ventilation. For genome-wide gene expression analysis, BEAS-2B cells (passage 41) were incubated with 10M-BM-5g/ml PM10 (school 4 indoor and outdoor) for 4, 10 or 24h, all in triplicate. experiment type : time course

Dataset Information

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

Publications

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

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