The association between inflammation, the microbiome and urethane-induced pulmonary adenocarcinoma

Lung cancer is amongst the most common types of cancer throughout the world. The overall 5-year survival rate is ~17%. A number of studies have demonstrated that the microbiome existing within the host may affect the level of inflammation, and consequently contribute to the carcinogenesis of certain types of cancer. To investigate the role of inflammation and the microbiome in the carcinogenesis of lung cancer, an intervention study involving mice, including a control group (C; n=5), a urethane-induced pulmonary adenocarcinoma group (U; n=5) and a prebiotics intervention group (P; n=5) was carried out. This pulmonary adenocarcinoma model was reviewed, and incidences of the disease were identified using histopathology. The levels of the inflammatory cytokines nuclear factor κB (NF-κB), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the sera samples were measured using an ELISA technique. In addition, high-throughput sequencing of the 16S ribosomal RNA gene segment was used to analyze the species present in the microbiome of the lower airways and intestinal tracts of mice. The results demonstrated that groups P and U exhibited altered histopathology and the development of lung adenocarcinoma tumors, but no differences were observed between the groups. The level of inflammation, determined by measuring the levels of NF-κB, TNF-α, IL-1β and IL-6 inflammatory cytokines, was significantly lower in group P compared with group U (P