Dynamic of apoptosis of cells in duodenal villi infected with Eimeria acervulina in broiler chickens

Abstract

The aim of our study was to evaluate the parasite -host interactions at apoptosis level. We studied histopathological changes and time course of apoptosis in the duodenum during Eimeria acervulina infection. One-day-old broiler chicks were randomly allocated into two equal groups. At the age of two weeks the first group was experimentally infected with a pure suspension of sporulated E. acervulina oocysts. The second group served as a negative control. Tissue samples from the upper part of duodenum were obtained at 0.5, 1, 2, 3, 4, 5 and 6 days post infection. Biopsies of duodenum were studied immunohistochemically using DeadEnd TM Colometric TUNEL System for apoptosis detection in duodenal mucosa. Number of parasites in duodenal epithelium was also investigated. Our experimental results demonstrate: (i) macroscopic and histopathological changes in epithelium detected mainly in proximal segment of duodenum in infected groups; (ii) the number of developmental stages of E. acervulina (DSEA) during our trial increased, reaching the maximum 5 days post infection (dpi) (332.2 ± 16.12) (mean ± SEM), whereas the amount of DSEA declined significantly as late as 6 dpi (124.6 ± 3.91); (iii) the highest apoptosis level was recorded in initiatory 0.5 dpi (13.2 ± 1.02) and on the end of parasite development cycle after 5 dpi (12.6 ± 1.36). Finally, results showed that there was a period of inhibition of apoptosis during infection by E. acervulina.

Eimeria tenellaROPkinaseEtROP1induces G0/G1 cell cycle arrest and inhibits host cell apoptosis

“…Purification of EtROP1-FLAG-containing complexes ( Figure 2d) and subsequent LC-MS/MS analysis identified approximately 29 proteins in the 55-kDa signal among which, the tumour protein p53 (protein ID gi_112489878; Table S1), modulating apoptosis in response to multiple stress signals (Levine, 1997). Our result, and previous observations reporting apoptosis inhibition in host cells infected by Eimeria (del Cacho, Gallego, Lopez-Bernad, Quilez, & Sanchez-Acedo, 2004;Lang, Kann, Zahner, Taubert, & Hermosilla, 2009;Major et al, 2011), prompted us to focus on this candidate. EtROP1-p53 interaction was further confirmed by a pull down experiment ( Figure 3).…”

“…EtROP1 is highly conserved between avian Eimeria species (43% to 92% identity, data not shown), and we may speculate that EtROP1 has crucial functions, probably shared by species infecting avian hosts. Interestingly, inhibition of host cell apoptosis by sporozoites has been described for E. tenella (del Cacho et al, ) but also for Eimeria bovis (Lang et al, ) and Eimeria acervulina (Major et al, ), which present, compared with the caecal species E . tenella , distinct sites of infection (ileum and duodenum, respectively) and distinct developmental cycles (21 and 5 days, respectively).…”

Anti-coccidial and anti-apoptotic activities of palm pollen grains on Eimeria papillata-induced infection in mice

“…Parasite invasion and replication may cause considerable stress to the host cell (Frias et al 2007;Fisch et al 2007) and this stress, in turn, trigger apoptosis (Green & Reed 1998;Green 2000). Other factors that contribute to apoptosis are the elevation of reactive oxygen and nitrogen intermediates and inflammatory cytokines within cells (Ramachanran et al 2000;Major et al 2011). Pollen extract exerts a strong activity against oxidative damage and inflammatory response (Kroyer & Hegedus 2001;Choi 2007;Le Blanca et al 2009) and hence inhibiting E. papillata induced apoptotic changes within infected mice jejuna.…”

Gene expression, oxidative stress and apoptotic changes in rabbit ileum experimentally infected with Eimeria intestinalis

“…Other factors that contribute to apoptosis during the course of eimeriosis are the elevation of reactive oxygen species and the presence of nitrogen intermediates and inflammatory cytokines within the infected cells (Major et al 2011, Metwaly et al 2014.…”