Departmental Bulletin Paper Immune cellular responses to Sendai virus infection in D2.B6-Sen1Sen2Sen3 congenic mice, of which three quantitative trait loci responsible for the resistance to infection were introgressed from C57BL/6 mouse into DBA/2 mouse

Abbas, Raghda M.F.  ,  Tag-EL-Din-Hassan, Hassan T.  ,  Boonyarattanasoonthorn, Tussapon  ,  Aoshima, Keisuke  ,  Morimatsu, Masami  ,  Agui, Takashi

66 ( 2 )  , pp.93 - 103 , 2018-05 , Faculty of Veterinary Medicine, Hokkaido University
ISSN:0047-1917
Description
It has been reported that C57BL/6 (B6) mice are resistant to the Sendai virus (SeV) infection, whereas DBA/2 (D2) mice are susceptible, the cause of susceptibility in D2 mice is hyper-inflammatory cytokine production, and three quantitative trait loci (QTLs), Sen1, Sen2, and Sen3 are identified to be responsible for this difference. We previously have verified that the introgression of B6-derived these three QTLs into D2-genetic background increases survival rate and suppresses cytokine production by generating D2.B6-Sen1Sen2Sen3 congenic mice. In this study, we investigated immune cellular responses of D2.B6-Sen1Sen2Sen3 mice after SeV infection. Body weight loss, viral load, immune cells in broncho-alveolar lavage fluid (BALF), and histopathological index of SeV-infected male D2. B6-Sen1Sen2Sen3 mice were comparable to those of B6 mice except for the number of neutrophils in BALF. In contrast, female D2.B6-Sen1Sen2Sen3 mice were divided into survived and non-survived mice after SeV infection. Viral load and macrophage number in BALF in SeV-infected female D2. B6-Sen1Sen2Sen3 mice were comparable to those of B6 mice, whereas the number of total cells, neutrophils, and lymphocytes in BALF were remained in the level of D2 mouse. There was a correlation between body weight loss and these immune cellular responses in SeV-infected female D2.B6-Sen1Sen2Sen3 mice. These results indicate that the introgression of B6 alleles of these three QTLs into D2-genetic background resulted in resistance to SeV infection by optimizing the aggressive immune cellular responses that seen in D2 mice, although there may be other loci responsible for difference between B6 and D2 mice.
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