Infection of Ixodes spp. tick cells with different XXXX isolates induces the inhibition of apoptotic cell death.

@entity1 @entity1641 @entity742 @entity235 @entity3966 @entity281 @entity221 @entity4210
@entity4210 is an intracellular rickettsial pathogen transmitted by Ixodes spp. ticks, which causes granulocytic anaplasmosis in @entity1 , @entity1641 and @entity235 and @entity221 ( @entity221 ) in ruminants. In the United States, @entity1 granulocytic anaplasmosis (HGA) is highly prevalent while @entity221 has not been reported. However, in Europe the situation is the opposite, with high prevalence for @entity221 in @entity742 and low prevalence of HGA. The origin of these differences has not been identified and our hypothesis is that different A. phagocytophilum isolates impact differently on tick vector capacity through inhibition of apoptosis to establish @entity281 of the tick vector. In this study we used three different isolates of A. phagocytophilum of @entity1 , @entity235 and ovine origin to infect the Ixodes ricinus-derived cell line IRE/CTVM20 and the @entity3966 -derived cell line ISE6 in order to characterize the effect of @entity281 on the level of tick cell apoptosis. Inhibition of apoptosis was observed by flow cytometry as early as 24h post- @entity281 for both tick cell lines and all three isolates of A. phagocytophilum, suggesting that pathogen @entity281 inhibits apoptotic pathways to facilitate @entity281 independently of the origin of the A. phagocytophilum isolate and tick vector species. However, @entity281 with A. phagocytophilum isolates inhibited the intrinsic apoptosis pathway at different levels in @entity3966 and I. ricinus cells. These results suggested an impact of vector-pathogen co-evolution on the adaptation of A. phagocytophilum isolates to grow in tick cells as each isolate grew better in the tick cell line derived from its natural vector species. These results increase our understanding of the mechanisms of A. phagocytophilum @entity281 and multiplication and suggest that multiple mechanisms may affect disease prevalence in different geographical regions.
