Characteristics of the gastritis induced by Listeria monocytogenes in mice: microbiology, histopathology, and mRNA expression of inflammatory mediators with time course of infection.

Listeria monocytogenes induces the suppurative gastritis in some mice strains. In this study, characteristics of the gastritis caused by L. monocytogenes infection in mice were examined with time course of infection. Mice were administered intragastrically with 1.8 x 10(8) CFU of L. monocytogenes. Each three mice were sacrificed by cervical dislocation at 1, 3, 5, 7, 10, 14, 17, 21, and 28 days postinoculation (pi), respectively. Bacterial colonization in the stomachs reached the peak at 3 days pi, maintained over 4.3 log10 CFU/g tissue until 14 days pi, and was cleared by 28 days pi. However, in the spleens and livers, the bacteria could not be detected after 7 days pi. The gastric lesions were the most prominent at between 3 and 7 days pi. The lesions consisted of marked neutrophilic infiltration, edema, vacuolar degeneration and necrosis of muscle cells and were more severe in the nonglandular region and fundus than in the pylorus, and were in submucosa, lamina muscularis, and serosa than in mucosa. mRNA expression of several cytokines (INF-gamma, IL-1beta, IL-5, IL-6, IL-12, and TNF-alpha) and chemokines (KC, MCP-1) increased in the gastric tissue of infected mice at 1-7 days pi and slightly decreased at 14 days pi. These findings would be useful for studying the pathological mechanism of human febrile gastroenteritis due to L. monocytogenes infection.