Yu-Jun Tang1, Han-Hsin Chang2, Chun-Yi Chiang3, Chane-Yu Lai4, Min-Yen Hsu5,6, King-Rong Wang7, Hsin-Hsuan Han4, Ling-Yun Chen1, David Pei-Cheng Lin3,5. 1. Institute of Biochemistry, Microbiology, and Immunology, Chung Shan Medical University, Taichung, Taiwan. 2. Department of Nutrition, Chung Shan Medical University, Taichung, Taiwan. 3. Department of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan. 4. Department of Occupational Safety and Health, Chung Shan Medical University, Taichung, Taiwan. 5. Department of Ophthalmology, Chung Shan Medical University Hospital, Taichung, Taiwan. 6. Department of Medicine, Chung Shan Medical University, Taichung, Taiwan. 7. Department of Psychology, Chung Shan Medical University, Taichung, Taiwan.
Abstract
Purpose: Several pieces of epidemiologic evidence have indicated PM2.5 (particulate matter with a diameter of 2.5 μm or less) as a causing factor of allergic conjunctivitis, but without experimental elucidation of mechanism. In the present study, PM2.5 in solution was directly applied to the mouse ocular surface to elucidate whether PM2.5 might cause allergic conjunctivitis, and its underlying mechanisms were analyzed. Methods: ICR mice were challenged for 18 consecutive days with eye drops containing PM2.5 at 3.2, 6.4, and 12.8 mg/mL in 0.9% NaCl saline, along with the controls prepared in parallel without PM2.5 and another control group treated with both PM2.5 at 12.8 mg/mL and artificial tears. On day 19, the whole eyes and meibomian glands were harvested for histopathological analyses and assessment of clinical scoring, tear volume, tear breakup time, and tear ferning. Furthermore, goblet cells by periodic acid Schiff stain and infiltrated eosinophils by Giemsa stain were quantified and compared among study groups. Results: Clinical scoring showed more eyelid edema, tearing, and scratching behaviors, with longer tear breakup time under the influence of increased PM2.5 concentrations. Tear ferning assay showed less tear crystal formation and decreased crystal branches after exposure to PM2.5. In addition, higher goblet cell density in the upper palpebral conjunctiva and extensive eosinophil infiltration in the entire conjunctiva and in the meibomian glands were induced by PM2.5. Conclusions: These results demonstrate that PM2.5 can induce symptoms similar to clinical allergic conjunctivitis and that the murine acute allergic conjunctivitis model can be induced by direct exposure to PM2.5.
Purpose: Several pieces of epidemiologic evidence have indicated PM2.5 (particulate matter with a diameter of 2.5 μm or less) as a causing factor of allergic conjunctivitis, but without experimental elucidation of mechanism. In the present study, PM2.5 in solution was directly applied to the mouse ocular surface to elucidate whether PM2.5 might cause allergic conjunctivitis, and its underlying mechanisms were analyzed. Methods: ICR mice were challenged for 18 consecutive days with eye drops containing PM2.5 at 3.2, 6.4, and 12.8 mg/mL in 0.9% NaCl saline, along with the controls prepared in parallel without PM2.5 and another control group treated with both PM2.5 at 12.8 mg/mL and artificial tears. On day 19, the whole eyes and meibomian glands were harvested for histopathological analyses and assessment of clinical scoring, tear volume, tear breakup time, and tear ferning. Furthermore, goblet cells by periodic acid Schiff stain and infiltrated eosinophils by Giemsa stain were quantified and compared among study groups. Results: Clinical scoring showed more eyelid edema, tearing, and scratching behaviors, with longer tear breakup time under the influence of increased PM2.5 concentrations. Tear ferning assay showed less tear crystal formation and decreased crystal branches after exposure to PM2.5. In addition, higher goblet cell density in the upper palpebral conjunctiva and extensive eosinophil infiltration in the entire conjunctiva and in the meibomian glands were induced by PM2.5. Conclusions: These results demonstrate that PM2.5 can induce symptoms similar to clinical allergic conjunctivitis and that the murine acute allergic conjunctivitis model can be induced by direct exposure to PM2.5.
Authors: Jun-Sang Bae; Soo Bin Oh; Jeongyun Kim; Hoon Kim; Ji Hye Kim; Eun-Hee Kim; Kyong Jin Cho; Ji-Hun Mo Journal: Allergy Asthma Immunol Res Date: 2022-01 Impact factor: 5.764