Airborne Particulate Matter Induces Nonallergic Eosinophilic Sinonasal Inflammation in Mice
Autor: | Thomas E. Sussan, Sanjay Rajagopalan, Murugappan Ramanathan, Sandra Y. Lin, Elina Toskala, Nitya Surya, Shyam Biswal, Nyall R. London, Xiaoquan Rao, Anuj Tharakan |
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Rok vydání: | 2017 |
Předmět: |
Male
Pulmonary and Respiratory Medicine Pathology medicine.medical_specialty Interleukin-1beta Clinical Biochemistry Fluorescent Antibody Technique Inflammation Nose Proinflammatory cytokine 03 medical and health sciences 0302 clinical medicine In vivo Paranasal Sinuses Eosinophilic Hypersensitivity medicine Animals Particle Size Respiratory system 030223 otorhinolaryngology Molecular Biology Original Research Interleukin-13 Inhalation business.industry Epithelial Cells Cell Biology Eosinophil Eosinophils Mice Inbred C57BL medicine.anatomical_structure 030228 respiratory system Immunology Interleukin 13 Particulate Matter medicine.symptom business |
Zdroj: | American Journal of Respiratory Cell and Molecular Biology. 57:59-65 |
ISSN: | 1535-4989 1044-1549 |
Popis: | Exposure to airborne particulate matter (PM) has been linked to aggravation of respiratory symptoms, increased risk of cardiovascular disease, and all-cause mortality. Although the health effects of PM on the lower pulmonary airway have been extensively studied, little is known regarding the impact of chronic PM exposure on the upper sinonasal airway. We sought to test the impact of chronic airborne PM exposure on the upper respiratory system in vivo. Mice were subjected, by inhalation, to concentrated fine (2.5 μm) PM 6 h/d, 5 d/wk, for 16 weeks. Mean airborne fine PM concentration was 60.92 μm/m3, a concentration of fine PM lower than that reported in some major global cities. Mice were then killed and analyzed for evidence of inflammation and barrier breakdown compared with control mice. Evidence of the destructive effects of chronic airborne PM on sinonasal health in vivo, including proinflammatory cytokine release, and macrophage and neutrophil inflammatory cell accumulation was observed. A significant increase in epithelial barrier dysfunction was observed, as assessed by serum albumin accumulation in nasal airway lavage fluid, as well as decreased expression of adhesion molecules, including claudin-1 and epithelial cadherin. A significant increase in eosinophilic inflammation, including increased IL-13, eotaxin-1, and eosinophil accumulation, was also observed. Collectively, although largely observational, these studies demonstrate the destructive effects of chronic airborne PM exposure on the sinonasal airway barrier disruption and nonallergic eosinophilic inflammation in mice. |
Databáze: | OpenAIRE |
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