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Particulate Matter Exposure Aggravates IL-17-Induced Eye and Nose Inflammation in an OVA/Poly(I:C) Mouse Model

PURPOSE: Data on the effects of direct particulate matter (PM) exposure on the eyes and the nose are limited. Here, an interleukin (IL)-17/neutrophil-dominant ovalbumin (OVA)/polyinosinic-polycytidylic acid (Poly(I:C)) mouse model was used to evaluate the effect of different-sized titanium dioxide (...

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Detalles Bibliográficos
Autores principales: Bae, Jun-Sang, Oh, Soo Bin, Kim, Jeongyun, Kim, Hoon, Kim, Ji Hye, Kim, Eun-Hee, Cho, Kyong Jin, Mo, Ji-Hun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Academy of Asthma, Allergy and Clinical Immunology; The Korean Academy of Pediatric Allergy and Respiratory Disease 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8724832/
https://www.ncbi.nlm.nih.gov/pubmed/34983107
http://dx.doi.org/10.4168/aair.2022.14.1.59
Descripción
Sumario:PURPOSE: Data on the effects of direct particulate matter (PM) exposure on the eyes and the nose are limited. Here, an interleukin (IL)-17/neutrophil-dominant ovalbumin (OVA)/polyinosinic-polycytidylic acid (Poly(I:C)) mouse model was used to evaluate the effect of different-sized titanium dioxide (TiO(2)) particles on the eyes and the nose. We also examined whether IL-17-neutralizing antibody (IL-17Ab) treatment could reverse TiO(2) effects. METHODS: The nasal cavities and conjunctival sacs of each mouse were challenged with OVA and Poly(I:C) to induce neutrophil-dominant inflammation and then exposed to micro- and nano-TiO(2). Subsequently, IL-17Ab was administered to investigate the role of IL-17 and inflammatory parameters. RESULTS: Micro- and nano-TiO(2) resulted in significant decreases in tear-break-up time and increases in corneal damage. Airborne micro-TiO(2) also increased nasal rubbing and sneezing counts compared with the OVA/Poly(I:C). Micro-TiO(2) exposure increased infiltration of neutrophils and IL-17A+ cells in the conjunctival tissues and the nasal mucosae. In addition, these increased symptoms and inflammation in the eyes and the nose by micro-TiO(2) exposure were inhibited by the IL-17Ab, suggesting IL-17 dependency. CONCLUSIONS: TiO(2) aggravated IL-17-induced eye and nose inflammation and the IL-17Ab alleviated inflammation in the OVA/Poly(I:C) mouse model. These results may help develop a therapeutic modality for PM exposure and provide evidence for PM-associated diseases.