Inhalation toxicology
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Inhalation toxicology · Jun 2009
Comparative StudyExposure to cigarette smoke upregulates AP-1 activity and induces TNF-alpha overexpression in mouse lungs.
Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary disease, and involves overexpression of many proinflammatory genes. Transcription factors regulating expression of inflammatory mediators may play a key role in characterizing the disease. To observe alterations in pulmonary function, observe pathological changes in lung tissues, and detect changes in transcriptional factors, mice were exposed to 30 days of cigarette smoke. ⋯ EMSA demonstrated that smoke exposure enhanced activator protein (AP)-1 DNA binding activation, but only slightly changed NF-kappaB activation in mouse lung. Compared to the control group, smoke exposure induced a notable increase in TNF-alpha in BALF. These data demonstrated that subacute smoke-triggered lung inflammation was accompanied by inflammatory cell influx, AP-1 activation, and proinflammatory gene overexpression in mouse lungs.