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 emphyse…
M Voss, B Wonnenberg, L Wolf, A Kamyschnikow, A Honecker, C Herr, R Bals, C Beisswenger · Pneumologie · 2015 · Heft 02
Bibliografische Angaben
Zusammenfassung
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-deficient mice and decreased in IκBα-deficient mice after acute cigarette smoke exposure. In the chronic CS model, assessment of pulmonary function showed that the total lung capacity was increased in room…