In summary, we believe that in a putative Fn-related disease scenario involving respiratory epithelial cells, whereby infection occurs along the respiratory tract (tracheal to bronchial to alveolar epithelial cells), Fn adherence (possible via fusobacterial adhesin) would serve as a potential virulence factor that would stimulate a host response involving inflammatory signals (secreted IL-8 and IL-6) that differ in each epithelial cell type. This evidence concerns the gene IL6 and infection.