Relationship between Lung Carcinogenesis and Chronic Inflammation in Rodents

Simple Summary Lung cancer is the most common cause of cancer-related deaths worldwide. There are various risk factors for lung cancer, including tobacco smoking, inhalation of dust particles, chronic inflammation, and genetic factors. Chronic inflammation has been considered a key factor that promotes tumor progression via production of cytokines, chemokines, cytotoxic mediators, and reactive oxygen species by inflammatory cells. Here, we review rodent models of lung tumor induced by tobacco, tobacco-related products, and pro-inflammatory materials as well as genetic modifications, and discuss the relationship between chronic inflammation and lung tumor. Through this review, we hope to clarify the effects of chronic inflammation on lung carcinogenesis and help develop new treatments for lung cancer. Lung cancer remains the leading cause of cancer-related deaths, with an estimated 1.76 million deaths reported in 2018. Numerous studies have focused on the prevention and treatment of lung cancer using rodent models. Various chemicals, including tobacco-derived agents induce lung cancer and pre-cancerous lesions in rodents. In recent years, transgenic engineered rodents, in particular, those generated with a focus on the well-known gene mutations in human lung cancer (KRAS, EGFR, and p53 mutations) have been widely studied. Animal studies have revealed that chronic inflammation significantly enhances lung carcinogenesis, and inhibition of inflammation suppresses cancer progression. Moreover, the reduction in tumor size by suppression of inflammation in animal experiments suggests that chronic inflammation influences the promotion of tumorigenesis. Here, we review rodent lung tumor models induced by various chemical carcinogens, including tobacco-related carcinogens, and transgenics, and discuss the roles of chronic inflammation in lung carcinogenesis.