Effects of host vimentin on Eimeria tenella sporozoite invasion

Background: Chicken coccidiosis is a parasitic disease caused by Eimeria of Apicomplexa, which has caused great economic loss to the poultry breeding industry. Host vimentin is a key protein in the process of infection of many pathogens. In an earlier phosphorylation proteomics study, we found that the phosphorylation level of host vimentin was significantly regulated after Eimeria tenella sporozoite infection. Therefore, we explored the role of host vimentin in the invasion of host cells by sporozoites. Methods: Chicken vimentin protein was cloned and expressed. We used qPCR, western blotting, and indirect immunofluorescence to detect levels of mRNA transcription, translation, and phosphorylation, and changes in the distribution of vimentin after E tenella sporozoite infection. The sporozoite invasion rate in DF-1 cells treated with vimentin polyclonal antibody or with small interfering RNA (siRNA), which downregulated vimentin expression, was assessed by an in vitro invasion test. Results: The results showed that vimentin transcription and translation levels increased continually at 6-72 h after E. tenella sporozoite infection, and the total phosphorylation levels of vimentin also changed. About 24 h after sporozoite infection, vimentin accumulated around sporozoites in DF-1 cells. Treating DF-1 cells with vimentin polyclonal antibody or down-regulating vimentin expression by siRNA significantly improved the invasion efficiency of sporozoites. Conclusion: In this study, we showed that vimentin played an inhibitory role during the invasion of sporozoites. These data provided a foundation for clarifying the relationship between Eimeria and the host.

Automated summary

In this study, we found that the transcription and translation levels of vimentin increased continuously after Eimeria tenella sporozoite infection in chickens, and the phosphorylation levels of vimentin also changed. Vimentin accumulated around sporozoites in host cells after infection, and inhibiting vimentin expression significantly improved the invasion efficiency of sporozoites.