Cytoskeletal changes in Eimeria bovis-infected host endothelial cells during first merogony

Abstract

The first merogony of Eimeria bovis takes place in lymphatic endothelial cells of the ileum, resulting in the formation of macromeronts up to 250 microm. In this study, we investigated the host cell cytoskeleton (actin filaments, microtubules, spectrin, vimentin intermediate filaments) associated with parasitic development in vitro by confocal laser scanning microscopy (CLSM) using primary bovine umbilical vein endothelial cells (BUVEC) and bovine spleen lymphatic endothelial cells (BSLEC) as host cells. No prominent changes in the host cell cytoskeleton were detected 1-3 days after E. bovis sporozoite invasion. With ongoing meront maturation a significant increase in microtubules and actin filaments close to the parasitophorous vacuole (PV) was found. Mature macromeronts within the PV were completely enclosed by these cytoskeletal elements. Our findings suggest, that in order to guarantee the survival of the host cell on the enlargement of macromeronts, E. bovis needs not only to augment but also to rearrange its cytoskeletal system.

A newly described strain of Eimeria arloingi (strain A) belongs to the phylogenetic group of ruminant-infecting pathogenic species, which replicate in host endothelial cells in vivo

“…A similar feature has also been suggested for the pathogenic species E. bovis and E. zuernii (Kawahara et al, 2010). It is intriguing to verify that despite the different host The phylogenetic proximity of E. arloingi and E. bovis may be in accordance with other common features of parasite-host cell interactions, such as the modulation of host cell-apoptosis (Lang et al, 2009), -cytoskeleton (Hermosilla et al, 2008) and -metabolism (Hamid et al, 2014;Hamid et al, 2015;Silva et al, 2015;Taubert et al, 2010) to guarantee successful macromeront formation.…”

Microarray-based transcriptional profiling ofEimeria bovis-infected bovine endothelial host cells

“…Hermosilla et al [16] reported an increasing influence on actin- and tubulin-related reorganisation of the host cell cytoskeleton with ongoing infection. We now found enhanced gene transcription of several tubulins (TUBB, TUBB4, TUBB6) and of molecules involved in microtubule binding or cytoskeleton organisation (TPPP, DOCK7, CKAP4, DCT3) in the late phase of infection.…”

“…This lengthy process (14–18 days) is associated with the enlargement and reorganisation of the host cell (e.g. host cell cytoskeletal elements [16]). Parasite growth and proliferation within the parasitophorous vacuole (PV) requires nutrients from the host cell, as in other apicomplexa [7, 27].…”

Apicomplexans pulling the strings: manipulation of the host cell cytoskeleton dynamics

“…This could serve the acquisition of organelles such as mitochondria and the endoplasm reticulum to the closer vicinity of the E. bovis PV during replication (Hermosilla et al . 2008). In E. bovis infected cells, the transcription levels of several tubulins (TUBB, TUBB4 and TUBB6) were increased.…”

“…Actin surrounds the PV within 3 dpi, and actin filament bundles form a thick layer in the final stages of meront maturation (15–20 dpi) (Hermosilla et al . 2008). Several actin-related genes are upregulated in cells containing developing macromeronts.…”