Rela and P50 in Airway Cells with or without E1a Transection, Chicken Soup or Jewish Medicine Etiology of Community-acquired Pneumonia Requiring Hospitalization in Japan

LPS could induce nuclear translocation of NF-kB in E1Atransfected cells alone.7 In E1A-transformed airway cells, the NF-kB transcription factor is involved in the IL-8 gene and ICAM-1 gene expression after LPS stimulation. In addition, Metcalf8 reported that adenovirus E1A 13S gene product upregulates TNF-a gene. On the other hand, cigarette smokers have increased numbers of neutrophils present in their lower respiratory tract. Acute exposure to cigarette smoke induces infiltration of neutrophils into the airways through NF-kB and IL-8 gene expression.9 Consequently, the latent adenovirus infection and cigarette smoke synergistically cause chronic airway inflammation through the cytokine genes and adhesion molecule genes expression, possibly via NF-kB activation. Thus, NF-kB activation may be involved in the pathogenesis of COPD and chronic airway inflammation after chronic cigarette smoke inhalation and adenovirus infection. These experimental data should be further confirmed in the future by clinical data in humans.