Adverse impact of acute Toxoplasma gondii infection on human spermatozoa.

Toxoplasma gondii is an obligate intracellular protozoan parasite that can infect virtually any nucleated cell within human and other endoderm animal tissue, including male reproductive organs. Herein, we investigate the capacity of T. gondii tachyzoites to infect and proliferate within the testes and epididymis and examine the resulting impact on human spermatozoa structure and functionality.

AMPK and CAMKK activation participate in early events of -triggered NET formation in bovine polymorphonuclear neutrophils.

is an obligate intracellular apicomplexan parasite that infects humans, eventually causing severe diseases like prenatal or ocular toxoplasmosis. also infects cattle but rarely induces clinical signs in this intermediate host type. So far, the innate immune mechanisms behind the potential resistance of bovines to clinical infections remain unclear.

Toxoplasma gondii infection induces early host cell cycle arrest and DNA damage in primary human host cells by a MYR1-dependent mechanism.

Toxoplasma gondii, an obligate intracellular parasite, control its host cell cycle through mechanisms that are not fully understood. Key effector molecules, including MYR1 and HCE1, play roles in translocating parasite proteins and inducing host cellular cyclin E1 overexpression, respectively. We investigated the early role of MYR1- and HCE1-driven host cell cycle arrest and DNA damage (up to 3 h p.

The CAMKK/AMPK Pathway Contributes to -Induced NETosis in Bovine Polymorphonuclear Neutrophils.

is an obligate intracellular apicomplexan parasite and the causal agent of bovine besnoitiosis. Bovine besnoitiosis has a considerable economic impact in Africa and Asia due to reduced milk production, abortions, and bull infertility. In Europe, bovine besnoitiosis is classified as an emerging disease.

Toxoplasma gondii modulates the host cell cycle, chromosome segregation, and cytokinesis irrespective of cell type or species origin.

Background: Toxoplasma gondii is an apicomplexan intracellular obligate parasite and the etiological agent of toxoplasmosis in humans, domestic animals and wildlife, causing miscarriages and negatively impacting offspring. During its intracellular development, it relies on nutrients from the host cell, controlling several pathways and the cytoskeleton. T.

infection-induced host cellular DNA damage is strain-dependent and leads to the activation of the ATM-dependent homologous recombination pathway.

is a globally occurring apicomplexan parasite that infects humans and animals. Globally, different typical and atypical haplotypes of induce varying pathologies in hosts. As an obligate intracellular protozoon, was shown to interfere with host cell cycle progression, leading to mitotic spindle alteration, chromosome segregation errors and cytokinesis failure which all may reflect chromosomal instability.

Me49 and NED strains arrest host cell cycle progression and alter chromosome segregation in a strain-independent manner.

is an obligate intracellular parasite that modulates a broad range of host cell functions to guarantee its intracellular development and replication. includes three classical clonal lineages exhibiting different degrees of virulence. Regarding the genetic diversity of circulating in Europe, type II strains and, to a lesser extent, type III strains are the dominant populations, both in humans and animals.

Dynamics of cell cycle proteins involved in -induced bovine NET formation.

Neutrophil extracellular traps (NET) formation is one important host innate defense mechanism elicited by polymorphonuclear neutrophils (PMN). NETs are composed by chromatin and proteins with microbicidal and signaling activity. So far, there is one report on triggered NETs in cattle, however, exact mechanisms, including signalling pathways and dynamics governing this reaction remain largely unknown.

Corrigendum: infection triggers S-phase arrest and alters nuclear characteristics in primary bovine endothelial host cells.

[This corrects the article DOI: 10.3389/fcell.2022.

Infection Triggers S-phase Arrest and Alters Nuclear Characteristics in Primary Bovine Endothelial Host Cells.

represents a major cause of abortive disease in bovines and small ruminants worldwide. As a typical obligate intracellular apicomplexan parasite, needs to modulate its host cell for successful replication. In the current study, we focused on parasite-driven interference with host cell cycle progression.

Glycolysis, monocarboxylate transport, and purinergic signaling are key events in -induced NETosis.

The protozoan parasite is the causative agent of bovine coccidiosis, an enteric disease of global importance that significantly affects cattle productivity. Previous studies showed that bovine NETosis-an important early host innate effector mechanism of polymorphonuclear neutrophil (PMN)-is elicited by stages. So far, the metabolic requirements of -triggered NET formation are unknown.

Novel Insights Into Sterol Uptake and Intracellular Cholesterol Trafficking During Macromeront Formation.

Apicomplexan parasites are considered as defective in cholesterol synthesis. Consequently, they need to scavenge cholesterol from the host cell by either enhancing the uptake of extracellular cholesterol sources or by upregulating host cellular biosynthesis. Given that macromeront formation in bovine lymphatic endothelial host cells is a highly cholesterol-demanding process, we here examined host parasite interactions based on host cellular uptake of different low-density lipoprotein (LDL) types, i.

Thiosemicarbazone Copper Chelator BLT-1 Blocks Apicomplexan Parasite Replication by Selective Inhibition of Scavenger Receptor B Type 1 (SR-BI).

Coccidian parasites are obligate intracellular pathogens that affect humans and animals. Apicomplexans are defective in de novo synthesis of cholesterol, which is required for membrane biosynthesis and offspring formation. In consequence, cholesterol has to be scavenged from host cells.

Morphometric analysis of aerobic Eimeria bovis sporogony using live cell 3D holotomographic microscopy imaging.

M onoxenous Eimeria species are widespread enteropathogenic apicomplexan protozoa with a high economic impact on livestock. In cattle, tenacious oocysts shed by E. bovis-infected animals are ubiquitously found and making infection of calves almost inevitable.

Macromeront Formation Induces Glycolytic Responses and Mitochondrial Changes in Primary Host Endothelial Cells.

is an intracellular apicomplexan parasite that causes considerable economic losses in the cattle industry worldwide. During the first merogony, forms large macromeronts with >140,000 merozoites I in host endothelial cells. Because this is a high-energy demanding process, exploits the host cellular metabolism to fulfill its metabolic requirements.

Canine -Induced Early Innate Immune Reactions Based on NETs Formation and Canine Vascular Endothelial Cell Activation In Vitro.

Due to its localization in the canine blood stream, is exposed to circulating polymorphonuclear neutrophils (PMN) and the endothelial cells of vessels. NETs release of canine PMN exposed to infective stages (third stage larvae, L3) and early pro-inflammatory immune reactions of primary canine aortic endothelial cells (CAEC) stimulated with L3-derived soluble antigens (Ag) were analyzed. Expression profiles of the pro-inflammatory adhesion molecules ICAM-1, VCAM-1, P-selectin and E-selectin were analyzed in Ag-stimulated CAEC.

Induces Polymorphonuclear Neutrophil Activation and Neutrophil Extracellular Traps Release.

trypomastigotes are classical blood parasites of cattle, these stages might become potential targets for circulating polymorphonuclear neutrophils (PMN). We here investigated NETs extrusion and related oxygen consumption in bovine PMN exposed to motile trypomastigotes . Parasite exposure induced PMN activation as detected by enhanced oxygen consumption rates (OCR), extracellular acidification rates (ECAR), and production of total and extracellular reactive oxygen species (ROS).

infections induce G cell cycle arrest and a senescence-like phenotype in endothelial host cells.

Apicomplexan parasites are well-known to modulate their host cells at diverse functional levels. As such, apicomplexan-induced alteration of host cellular cell cycle was described and appeared dependent on both, parasite species and host cell type. As a striking evidence of species-specific reactions, we here show that Eimeria bovis drives primary bovine umbilical vein endothelial cells (BUVECs) into a senescence-like phenotype during merogony I.

Besnoitia besnoiti-driven endothelial host cell cycle alteration.

Besnoitia besnoiti is an important obligate intracellular parasite of cattle which primarily infects host endothelial cells of blood vessels during the acute phase of infection. Similar to the closely related parasite Toxoplasma gondii, B. besnoiti has fast proliferating properties leading to rapid host cell lysis within 24-30 h p.

Publisher Correction: α-SNAP is expressed in mouse ovarian granulosa cells and plays a key role in folliculogenesis and female fertility.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Optimized excystation protocol for ruminant Eimeria bovis- and Eimeria arloingi-sporulated oocysts and first 3D holotomographic microscopy analysis of differing sporozoite egress.

Successful excystation of sporulated Eimeria spp. oocysts is an important step to acquire large numbers of viable sporozoites for molecular, biochemical, immunological and in vitro experiments for detailed studies on complex host cell-parasite interactions. An improved method for excystation of sporulated oocysts and collection of infective E.

Histone H2A and Bovine Neutrophil Extracellular Traps Induce Damage of -Infected Host Endothelial Cells but Fail to Affect Total Parasite Proliferation.

tachyzoites infect and develop in bovine endothelial cells in vivo and trigger the release of neutrophil extracellular traps (NETs) from bovine polymorphonuclear neutrophils (PMN). The purpose of this study was to analyze if pure tachyzoite-triggered NETs would damage endothelial host cells and subsequently influence intracellular development and proliferation of tachyzoites in primary bovine endothelial cells. For comparison purposes, isolated A23187-induced NETs were also used.