Avian coccidiosis is due to highly prevalent Apicomplexa parasite Eimeria infection and results in significant production losses worldwide (3 billion per year). Optimization of coccidiosis prophylaxis suffers from gaps in knowledge of host-pathogen interactions. Elucidating the signalling-pathways manipulated by pathogen would decipher the way pathogens hijack, circumvent or suppress immune responses to favour their development and dissemination in the host. The project aims at identifying how secreted virulence determinants, such as rhoptry kinases, are involved in manipulating signalling pathways to pave the way for new control strategies.
EtROP1 is a virulence determinant produced by Eimeria tenella in host cells, during and early after cell invasion. We will compare transcriptomic analyses of non-infected avian cells with avian cells infected either with WT strain or with modified strain that overexpresses EtROP1. We will also study by-stander cells from both infected conditions to determine possible in trans effect of infection. We will use an avian epithelial cell model developed in our lab. Avian cells will be FACS sorted by fluorescent marker in order to reduce background noise from non-infected cells. This analysis will allow us to assess Eimeria tenella infection (and specific EtROP1 effects) on host cell transcription and possibly identify host signalling pathways modified by the parasite (and by EtROP1). These signalling pathways will pave the way to the identification of potential host protein targeted by parasite virulence factor EtROP1.
