Real-time PCR and western blotting results suggested that sustained exposure to H. pylori reduced the levels of JNK and JUN phosphorylation that were increased after short-term infection with H. pylori. All the data showed that H. pylori colonized in the gastric mucosa regulates the inflammatory response through TLR6/JNK signaling pathway induced by the bacteria. The gene discussed is JUN; the disease is infection.