Bovine herpes virus type 4 alters TNF-α and IL-8 profiles and impairs the survival of bovine endometrial epithelial cells

Reprod Biol. 2017 Sep;17(3):225-232. doi: 10.1016/j.repbio.2017.05.006. Epub 2017 May 22.

Abstract

Bovine herpes virus type 4 (BoHV-4) can be transmitted by contaminated semen to cows at the time of breeding and may cause uterine disease. The aim of this study was to characterize the susceptibility of bovine endometrial epithelial cells (bEEC) to BoHV-4 by using an in vitro model. When bEEC were challenged with different multiplicity of infection (MOI; from 0.001 to 10) of BoHV-4 for 6days, a significant decrease in cell survival with increasing MOI was observed. The bEEC were subsequently challenged with BoHV-4 MOI 0.1 for 7days. During the first 4days, numbers increased in a similar way in controls and infected group (p<0.01 when compared to Day 0). After Day 4, numbers of live cells in infected samples decreased when compared to controls and were lower than control at Day 7 (p<0.01). From titration and qPCR, increasing number of viral particles was observed from Day 1, and reached a plateau at Day 5. Concentrations of IL-8 increased with time and were higher in supernatants from infected cells than in controls (p<0.0001). TNF-α concentrations presented similar profile as cell survival ones. In conclusion, the survival of bEEC was strongly impaired by BoHV-4 infection in a time and dose dependent manner and supernatant cytokine profiles were altered. This information supports BoHV-4 implication in clinical cases of uterine diseases and the existence of a risk of BoHV-4 transmission from infected males through animal breeding.

Keywords: Cattle; Cell survival; Cytokine; Endometrial cell; Herpesvirus.

MeSH terms

  • Animals
  • Cattle*
  • Cells, Cultured
  • Endometrium / cytology*
  • Epithelial Cells / metabolism*
  • Epithelial Cells / virology
  • Female
  • Herpesvirus 4, Bovine*
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism*
  • Transcriptome
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Interleukin-8
  • Tumor Necrosis Factor-alpha