UFP, due to their large surface area, have enhanced capabilities to produce reactive oxygen species. For adult asthmatics, ambient levels of UFP (aerodynamic diameter <0.1 μm) were found to have a higher specific toxicological role compared to larger particles. There is rapidly increasing epidemiological evidence associating respiratory health effects and exposures to ultrafine particles (UFP) in a susceptible population, such as elderly, young children, and people with pre-existing respiratory conditions. Our findings demonstrate that oxidative stress plays an important role in EC-UFP-induced augmentation of functional and morphological alterations of Clara cells in allergic lung inflammation. NAC strongly reduced both functional and morphological alterations of Clara cells. In sensitized mice, inhalation of EC-UFP prior to OVA challenge caused most significant alterations of BALF and serum CC16 concentration, BALF total protein and TNF-α relative expression compared to relevant controls their Clara cells displayed the strongest morphological alterations and strongest goblet cell metaplasia occurred in the small airways. In non sensitized mice EC-UFP inhalation caused alterations in CC16 concentration, both at protein and mRNA level, and induced Clara cell hyperplasia. A morphometrical analysis of mucus hypersecretion and electron microscopy served to investigate goblet cell metaplasia and Clara cell morphological alterations. The relative expression of CC16 and TNF-α mRNA were measured in lung homogenates. CC16 was measured up to one week after allergen challenge in bronchoalveolar lavage fluid (BALF) and in serum. Ovalbumin (OVA)-sensitized mice were exposed to EC-UFP (507 μg/m 3 for 24 h) or filtered air immediately prior to allergen challenge and systemically treated with N-acetylcysteine (NAC) or vehicle prior and during EC-UFP inhalation. The purpose of the study was to investigate the role of elemental carbon ultrafine particles (EC-UFP)-induced oxidative stress on Clara cells and CC16 in a mouse model of allergic lung inflammation. Clara cell protein (CC16), the main secretory product of bronchiolar Clara cells, plays an important protective role in the respiratory tract against oxidative stress and inflammation.
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