Pathogenesis of the Influenza Virus in Diabetes Model Mice
Morihiro Ito *
Department of Biomedical Sciences, College of Life and Health Science, Chubu University, Aichi, Japan.
Hiromichi Kubota
Department of Biomedical Sciences, College of Life and Health Science, Chubu University, Aichi, Japan.
Tamaki Takeuchi
Department of Biomedical Sciences, College of Life and Health Science, Chubu University, Aichi, Japan.
Shanlou Qiao
Department of Biomedical Sciences, College of Life and Health Science, Chubu University, Aichi, Japan.
Masato Tsurudome
Department of Microbiology and Molecular Genetics, Mie University Graduate School of Medicine, Tsu, Mie, Japan.
Hideki Tsumura
Division of Laboratory Animal Resources, National Research Institute for Child Health and Development, Tokyo, Japan.
Akio Matsuda
Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.
Yasuhiko Ito
Department of Biomedical Sciences, College of Life and Health Science, Chubu University, Aichi, Japan.
*Author to whom correspondence should be addressed.
Abstract
When diabetes model mice and control mice were intranasally infected with the influenza virus (1 LD50), a significant higher mortality rate was observed in the diabetes model. The mortality rate became 100% at 10 days post infection. Furthermore, histopathological examination of lung tissue revealed a more enhanced inflammatory response in the diabetes model mice infected with the influenza virus. On the contrary, viral clearance from the lungs was suppressed in the diabetes model mice. The recruitment of macrophages was observed in the case of virus-infected control mice at 1 and 3 days post infection. Intriguingly, the number of macrophage in the lungs was not changed through the period of observation, thus the recruitment of macrophages in the lungs was not found in the virus-infected diabetes model mice.
Keywords: Influenza virus, diabetes model mice, pathogenesis