ArticleParasitology research2016
Besnoitia besnoiti infections activate primary bovine endothelial cells and promote PMN adhesion and NET formation under physiological flow condition.
Article in Parasitology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
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- A Review of the Neutrophil Extracellular Traps (NETs) from Cow, Sheep and Goat Models.International journal of molecular sciences · 2021Review
- Identification of molecular biomarkers associated with disease progression in the testis of bulls infected with Besnoitia besnoiti.Veterinary research · 2021Article
- CanineBiology · 2021Article
- Multiple Origins of Extracellular DNA Traps.Frontiers in immunology · 2021Review
- Besnoitia besnoiti-driven endothelial host cell cycle alteration.Parasitology research · 2020Article
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- RNA-Seq Analyses Reveal That Endothelial Activation and Fibrosis Are Induced Early and Progressively byFrontiers in cellular and infection microbiology · 2020Article
- Lytic cycle of Besnoitia besnoiti tachyzoites displays similar features in primary bovine endothelial cells and fibroblasts.Parasites & vectors · 2019Article
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- Immune response profile of caruncular and trophoblast cell lines infected by high- (Nc-Spain7) and low-virulence (Nc-Spain1H) isolates of Neospora caninum.Parasites & vectors · 2019Article
- Simultaneous and Positively Correlated NET Formation and Autophagy inFrontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Besnoitia besnoiti is an obligate intracellular and emerging coccidian parasite of cattle that mainly infects host endothelial cells during acute infection. We here analyzed early innate immune reactions of B. besnoiti-infected primary bovine umbilical vein endothelial cells (BUVEC). B. besnoiti infections significantly activated BUVEC since the gene transcripts of several adhesion molecules (P-selectin, intercellular adhesion molecule 1(ICAM-1)), chemokines (CXCL1, CXCL8, CCL5), and of COX-2 were significantly upregulated during in vitro infection. Overall, the highest upregulation of most transcripts was observed at 24 or 48 h post infection (p.i.). Enhanced adhesion molecule expression in infected host cells was confirmed by PMN adhesion assays being performed under physiological flow conditions revealing a significantly increased PMN adhesion on B. besnoiti-infected BUVEC layers at 24 h p.i. Furthermore, we were able to illustrate neutrophil extracellular traps (NETs) being released by PMN under physiological flow conditions after adhesion to B. besnoiti-infected BUVEC layers. The present study shows that B. besnoiti infections of primary BUVEC induce a cascade of pro-inflammatory reactions and triggers early innate immune responses.
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