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Article

Exposure to Traffic-Related Particulate Matter 2.5 Triggers Th2-Dominant Ocular Immune Response in a Murine Model

1
Department of Ophthalmology, Eunpyeong St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul 03312, Korea
2
Department of Environmental Engineering, Inha University, Incheon 22212, Korea
3
Department of Ophthalmology, Hallym University Dongtan Sacred Heart Hospital, College of Medicine, Hallym University, Gyeonggi-do 18450, Korea
*
Author to whom correspondence should be addressed.
Int. J. Environ. Res. Public Health 2020, 17(8), 2965; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17082965
Received: 27 March 2020 / Revised: 18 April 2020 / Accepted: 20 April 2020 / Published: 24 April 2020
(This article belongs to the Section Environmental Health)
Ambient particulate matter (PM), a major component of air pollution, aggravates ocular discomfort and inflammation, similarly to dry eye disease (DED) or allergies. However, the mechanism(s) by which PM induces the ocular inflammatory response is unknown. This study investigated the immunological response of traffic-related fine particulate matter (PM2.5) on the ocular surface in a murine model. C57BL/6 mice were exposed by topical application to PM2.5 or vehicle for 14 days to induce experimental environmental ocular disease. Corneal fluorescein staining and the number of ocular inflammatory cells were assessed in both groups. The expression of IL-1β, IL-6, tumor necrosis factor (TNF)-α, and mucin 5AC (MUC5AC) in the ocular surface were evaluated by real-time PCR. An immunohistochemical assay evaluated apoptosis and goblet cell density. ELISA was used to determine the levels of serum IgE and cytokines of Type 1 helper (Th1) and Type 2 helper (Th2) cells after in vitro stimulation of T cells in the draining lymph nodes (LNs). Exposure to traffic-related PM2.5 significantly increased corneal fluorescein staining and cellular toxicity in the corneal epithelium compared with the vehicle control. A significant increase in the number of CD11b+ cells on the central cornea and mast cells in the conjunctiva was observed in the PM2.5 group. Exposure to PM2.5 was associated with a significant increase in the corneal or conjunctival expression of IL-1β, IL-6, TNF, and MUC5AC compared to the vehicle, and increased maturation of dendric cells (DCs) (MHC-IIhighCD11c+) in draining LNs. In addition, PM2.5 exposure increased the level of serum IgE and Th2 cytokine production in draining LNs on day 14. In conclusion, exposure to traffic-related PM2.5 caused ocular surface damage and inflammation, which induced DC maturation and the Th2-cell-dominant allergic immune response in draining LNs. View Full-Text
Keywords: air pollution; allergic conjunctivitis; dendritic cell (DC); dry eye disease (DED); particulate matter (PM) air pollution; allergic conjunctivitis; dendritic cell (DC); dry eye disease (DED); particulate matter (PM)
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MDPI and ACS Style

Lee, H.S.; Han, S.; Seo, J.-W.; Jeon, K.-J. Exposure to Traffic-Related Particulate Matter 2.5 Triggers Th2-Dominant Ocular Immune Response in a Murine Model. Int. J. Environ. Res. Public Health 2020, 17, 2965. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17082965

AMA Style

Lee HS, Han S, Seo J-W, Jeon K-J. Exposure to Traffic-Related Particulate Matter 2.5 Triggers Th2-Dominant Ocular Immune Response in a Murine Model. International Journal of Environmental Research and Public Health. 2020; 17(8):2965. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17082965

Chicago/Turabian Style

Lee, Hyun S., Sehyun Han, Jeong-Won Seo, and Ki-Joon Jeon. 2020. "Exposure to Traffic-Related Particulate Matter 2.5 Triggers Th2-Dominant Ocular Immune Response in a Murine Model" International Journal of Environmental Research and Public Health 17, no. 8: 2965. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17082965

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