We are analyzing https://link.springer.com/article/10.1007/s00436-016-4941-5.

Title:
Besnoitia besnoiti infections activate primary bovine endothelial cells and promote PMN adhesion and NET formation under physiological flow condition | Parasitology Research
Description:
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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Keywords {🔍}

pubmed, article, google, scholar, cas, endothelial, besnoitia, central, cells, adhesion, besnoiti, bovine, hermosilla, taubert, neutrophil, extracellular, parasitol, vet, traps, res, toxoplasma, pmn, formation, infection, immune, gondii, host, cell, disease, besnoitiosis, eimeria, immunol, infections, cattle, gene, expression, silva, research, infected, schares, data, parasitology, parasite, innate, molecules, molecule, access, zahner, cortes, transcription,

Topics {✒️}

granulocyte-macrophage colony-stimulating factor month download article/chapter pro-inflammatory molecules e-selectin real-time quantitative pcr primary buvec induce real-time pcr data tnf-alpha gene transcription host endothelial cells besnoiti-infected buvec layers bovine endothelial cells tumor necrosis factor-alpha netosis-mediated cell death endothelial cells infected besnoitia besnoiti—experimental infection microarray-based transcriptional profiling vascular endothelial cells perforin-mediated immune responses infected host cells pmn-mediated immune reactions human endothelial cells besnoitia besnoiti infections 2-delta-delta-ct method ifn-gamma-mediated expression full article pdf chemokine gene transcription neutrophil extracellular traps central nervous system endothelial cell biology besnoitia besnoiti infection endothelial surface layer innate immune reaction physiological flow condition vascular adhesion molecules bovine umbilical cords central-eastern europe innate immune reactions european economic area privacy choices/manage cookies neospora caninum infections physiological flow conditions pro-inflammatory reactions 4 cyst-forming coccidia stewart cn jr eimeria bovis intermediate host species related subjects promote pmn adhesion pmn adhesion assays subsequent pmn adhesion bovine skin biopsies

Questions {❓}

Brinkmann V, Zychlinsky A (2012) Neutrophil extracellular traps: is immunity the second function of chromatin?

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         description: 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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         dateModified:2016-02-05T00:00:00Z
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            Adhesion molecules
            Chemokines
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            NET formation
            Medical Microbiology
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      description: 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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         Adhesion molecules
         Chemokines
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         NET formation
         Medical Microbiology
         Microbiology
         Immunology
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