Publications by authors named "Conejeros I"

Bovine besnoitiosis is a re-emerging cattle disease caused by the apicomplexan parasite , which severely affects individual animal welfare and profitability in cattle industry. We recently showed that tachyzoite exposure to bovine polymorphonuclear neutrophils (PMN) effectively triggers neutrophil extracellular trap (NET) formation, leading to parasite immobilization hampering host cell infection. So far, the triggers of this defense mechanism remain unclear.

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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.

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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.

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Cryptosporidiosis in humans is caused by infection of the zoonotic apicomplexan parasite . In 2006, it was included by the World Health Organization (WHO) in the group of the most neglected poverty-related diseases. It is characterized by enteritis accompanied by profuse catarrhalic diarrhea with high morbidity and mortality, especially in children of developing countries under the age of 5 years and in HIV patients.

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Article Synopsis
  • Bovine besnoitiosis is caused by a parasite and triggers neutrophil extracellular trap (NET) formation as an immune response, but the role of ATP in this process is not well understood.
  • Research shows that exposure to tachyzoites doesn't affect overall ATP levels in bovine neutrophils but does enhance their oxygen consumption and leads to increased NET formation, particularly when ATPγS is added.
  • The study identifies the P2X1 purinergic receptor as crucial for NET formation and neutrophil clustering in response to the parasite, while other purinergic receptors do not appear to influence this process.
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Article Synopsis
  • Cryptosporidiosis, caused by an apicomplexan parasite, is a major diarrheal pathogen in calves and contributes to significant economic losses and health issues in both livestock and children.
  • Neonatal bovine polymorphonuclear neutrophils (PMN) can form neutrophil extracellular traps (NETs) to combat this parasite, demonstrating their role in the innate immune response.
  • This study reveals that neonatal bovine PMN's NETosis is triggered by the parasite and is dependent on the P2X1 receptor, suggesting its potential as a mechanism for controlling cryptosporidiosis.
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The apicomplexan protozoan parasite is responsible for cryptosporidiosis, which is a zoonotic intestinal illness that affects newborn cattle, wild animals, and people all over the world. Mammalian monocytes are bone marrow-derived myeloid leukocytes with important defense effector functions in early host innate immunity due to their ATP purinergic-, CD14- and CD16-receptors, adhesion, migration and phagocytosis capacities, inflammatory, and anti-parasitic properties. The formation of monocyte extracellular traps (METs) has recently been reported as an additional effector mechanism against apicomplexan parasites.

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Colostrum is one of the most important factors influencing the health and development of mammalian neonates. It is well-established that leukocytes, including polymorphonuclear neutrophils (PMN), migrate from the mother to the infant via colostrum uptake. In this study, for the first time, we studied the ability of ovine colostral-derived PMN to extrude neutrophil extracellular traps (NETs) against the abortive apicomplexan parasite .

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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.

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Neospora caninum represents an obligate intracellular apicomplexan parasite of the family Sarcocystidae causing severe reproductive disorders in cattle, small ruminants, wild animals and canids worldwide. Neutrophil extracellular traps (NETs) were recently described as effective host defense mechanism of polymorphonuclear neutrophils (PMN) derived from cattle, dogs, goats and dolphins against N. caninum tachyzoites.

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Rat basophilic leukaemia (RBL) cells have been used for decades as a model of high-affinity Immunoglobulin E (IgE) receptor (FcεRI) signalling. Here, we describe the generation and use of huNPY-mRFP, a new humanised fluorescent IgE reporter cell line. Fusion of Neuropeptide Y (NPY) with monomeric red fluorescent protein (mRFP) results in targeting of fluorescence to the granules and its fast release into the supernatant upon IgE-dependent stimulation.

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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.

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Study Question: Does oxidative stress (OS) activate autophagy in human sperm?

Summary Answer: Human spermatozoa subjected to OS activate an autophagic response.

What Is Known Already: Autophagy is a regulated pathway of lysosomal degradation which helps eukaryotic cells to maintain or restore homeostasis, being a cellular stress response mechanism. OS is a main cause of impaired sperm function and is linked to male infertility; however, whether OS activates autophagy in human spermatozoa is unknown.

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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.

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Neospora caninum represents an obligate intracellular parasite that belongs to the phylum Apicomplexa and is a major abortive agent in bovines. During merogony, N. caninum tachyzoites invade and proliferate in host cells in vivo, including endothelial cells of lymphatic and blood vessels.

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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.

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Background: Bovine polymorphonuclear neutrophils (PMN) constitutively express the Toll-like receptors (TLRs) TLR2 and TLR4 and have been shown to generate Neutrophil extracellular traps (NETs) upon exposure to . The present work investigated the role of TLR2 and TLR4 in the recognition and uptake of sporozoites, IL-8 production and neutrophil extracellular trap (NET) formation.

Methods: TLR expression was performed by flow cytometric analysis on PMN exposed to live carboxyfluorescein succinimidyl ester (CFSE)-stained sporozoites.

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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).

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Fasciola hepatica is the causative agent of fasciolosis, a worldwide distributed zoonotic disease, leading to hepatitis in humans and livestock. Newly excysted juveniles (NEJ) of F. hepatica are the first invasive stages to encounter leukocytes of host innate immune system in vivo.

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Purpose: To study the effector mechanism against pathogens of polymorphonuclear neutrophils (PMN) and macrophages, called ETosis, involving the release of extracellular traps (ETs) in patients with acute epididymitis. To assess the different ET phenotypes present in semen samples and to identify correlations between ETosis and clinical parameters.

Materials And Methods: Samples from patients diagnosed with acute epididymitis were examined and compared with samples from uninfected controls.

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Deposition of sperm during artificial insemination in the bovine female reproductive tract results in early host innate immune reactions of polymorphonuclear neutrophils (PMNs). Furthermore, sperm-mediated neutrophil extracellular trap (NET) formation (NETosis) was recently reported to occur in different mammalian species, including humans. We, here, investigated the interactions of bovine PMN with different semen-derived samples and analyzed in more depth molecular aspects of this effector mechanism.

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Besnoitia besnoiti is the causative agent of bovine besnoitiosis, a disease affecting both, animal welfare and cattle productivity. NETosis represents an important and early host innate effector mechanism of polymorphonuclear neutrophils (PMN) that also acts against B. besnoiti tachyzoites.

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Toxoplasma gondii is a cosmopolitan zoonotic parasite and nowadays considered as an emerging neozoan pathogen in the marine environment. Cetacean innate immune reactions against T. gondii stages have not yet been investigated.

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