initiation of systemic inflammatory response. This study aimed to optimize the intestinal inflammation mouse model by injecting different doses of LPS. Methods: The experimental mice were induced by the intraperitoneal administration of 5, 10 and 20 mg/kg of LPS. After 12 hours, disease activity index (DAI) was evaluated by 2 different researchers with blinded test. Then, serum and colon tissues were obtained after sacrifice. Hematoxylin and eosin staining was performed to analyze the damage of intestinal tissues. Serum monocyte chemoattractant protein-1 (MCP-1) was estimated by enzyme-linked immunosorbent assay. Results: Injection with the 5, 10 and 20 mg/kg of LPS resulted in the increases of DAI score with the changes of fetal status such as diarrhea and hematochezia. However, there was no dose-dependent changes according to the doses of LPS. In addition, the colon length was not changed depends on the doses of LPS. The histopathological grades including intestinal barrier disruption, inflammatory cell infiltration and shape of villi were significantly increased by LPS injection. Moreover, serum MCP-1 levels were markedly increased with the concentrations of LPS. Conclusion: Taken together, LPS effectively induced the intestinal inflammation accompanied with the increment of serum chemokine and destruction of barrier.