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Alessandrini, F. ; Weichenmeier, I. ; van Miert, E.* ; Takenaka, S. ; Karg, E.W. ; Blume, C. ; Mempel, M. ; Schulz, S. ; Bernard, A.* ; Behrendt, H.

Effects of ultrafine particles-induced oxidative stress on Clara cells in allergic lung inflammation.

Part. Fibre Toxicol. 7:11 (2010)
Verlagsversion Volltext DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
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. 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.METHODS: Ovalbumin (OVA)-sensitized mice were exposed to EC-UFP (507 microg/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. CC16 was measured up to one week after allergen challenge in bronchoalveolar lavage fluid (BALF) and in serum. The relative expression of CC16 and TNF-alpha mRNA were measured in lung homogenates. A morphometrical analysis of mucus hypersecretion and electron microscopy served to investigate goblet cell metaplasia and Clara cell morphological alterations.RESULTS: In non sensitized mice EC-UFP inhalation caused alterations in CC16 concentration, both at protein and mRNA level, and induced Clara cell hyperplasia. 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-alpha relative expression compared to relevant controls; their Clara cells displayed the strongest morphological alterations and strongest goblet cell metaplasia occurred in the small airways. NAC strongly reduced both functional and morphological alterations of Clara cells.CONCLUSION: Our findings demonstrate that oxidative stress
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter PARTICULATE AIR-POLLUTION; CARBON-BLACK PARTICLES; TUMOR-NECROSIS-FACTOR; 16 KDA PROTEIN; SECRETORY PROTEIN; N-ACETYLCYSTEINE; CIGARETTE-SMOKE; ASTHMA; SERUM; MODEL
ISSN (print) / ISBN 1743-8977
e-ISSN 1743-8977
Zeitschrift Particle and Fibre Toxicology
Quellenangaben Band: 7, Heft: , Seiten: , Artikelnummer: 11 Supplement: ,
Verlag BioMed Central
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) CCG Environmental Dermatology and Allergology (ILBD-KAU)
Institute of Epidemiology (EPI)
Institute of Lung Biology (LHI)
Institute of Ecological Chemistry (IOEC)
Cooperation Group Comprehensive Molecular Analytics (CMA)