Objective: Tumor necrosis factor (TNF) is a vital cytokine involved in inflammation, immunity, and cellular organization.TNF secreted by tumor or tumor stromal cells has been reported as an important regulator in the tumor microenvironment and has been implicated in inflammation-associated tumor progression.According to our previous studies, TNF gene expression increased to 17.5 fold in the K-ras mutant lung cancer mice model (CC-LR) compared with the wild-type control.After exposure to non-typeable Hemophilus influenza(NTHi), which is found in the lower respiratory tract of chronic obstructive pulmonary disease (COPD) patients, the TNF levels in bronchoalveolar lavage fluid (BALF) of CC-LR mice increased5.3 fold.This condition resulted in a significant increase in lung surface tumor number (3.5 fold).