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Interferences in myeloid NF-κB signaling affects the inflammatory phenotype after acute smoke exposure and worsens lung damage in a murine model of cigarette smoke-induced emphysema

M Voss, B Wonnenberg, L Wolf, A Kamyschnikow, A Honecker, C Herr, R Bals, C Beisswenger · Pneumologie · Ausgabe 02/2015

DOI 10.1055/s-0035-1544600

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Autor:innenM Voss, B Wonnenberg, L Wolf, A Kamyschnikow, A Honecker, C Herr, R Bals, C Beisswenger
ZeitschriftPneumologie
Ausgabe02/2015
Jahrgang / SeitenNicht angegeben

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Abstract-Vorschau

Cigarette smoking is the main risk factor for the chronic obstructive pulmonary disease (COPD). It was the aim of this study to examine the function of myeloid cell nuclear factor-κB (NF-κB) in cigarette smoke (CS) induced lung inflammation and lung damage. We exposed wild type mice and mice deficient for myeloid RelA/p65 or myeloid IκBα to acute or chronic CS. Numbers of macrophages were increased in RelA/p65-defic…

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Zitierempfehlung

M Voss, B Wonnenberg, L Wolf, A Kamyschnikow, A Honecker, C Herr, R Bals, C Beisswenger (2015) Interferences in myeloid NF-κB signaling affects the inflammatory phenotype after acute smoke exposure and worsens lung damage in a murine model of cigarette smoke-induced emphysema. Pneumologie (02). https://doi.org/10.1055/s-0035-1544600

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