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    Effects of a pathogenic ETEC strain and a probiotic Enterococcus faecium strain on the inflammasome response in porcine dendritic cells (2018)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Loss, Henriette (WE 2)
    Aschenbach, Jörg R (WE 2)
    Ebner, Friederike (WE 6)
    Tedin, Karsten (WE 7)
    Lodemann, Ulrike (WE 2)
    Quelle
    Veterinary immunology and immunopathology
    Bandzählung: 203
    Seiten: 78 – 87
    ISSN: 0165-2427
    Sprache
    Englisch
    Verweise
    DOI: 10.1016/j.vetimm.2018.08.004
    Pubmed: 30143242
    Kontakt
    Institut für Mikrobiologie und Tierseuchen

    Robert-von-Ostertag-Str. 7-13
    14163 Berlin
    +49 30 838 51843 / 66949
    mikrobiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Dendritic cells (DC) are crucial for maintaining intestinal homeostasis and generating proper immune responses to bacteria occurring in the gut. Microbial stimuli can be recognized by intracellular receptors called inflammasomes, e.g., nucleotide oligomerization domain (NOD)-like receptor protein 3 (NLRP3). The aim of the present study was to unravel the inflammasome response of porcine monocyte-derived DC (MoDC). We investigated the capacity of probiotic Enterococcus faecium NCIMB 10415 (E. faecium) and enterotoxigenic Escherichia coli (ETEC) to elicit inflammasome activation. Since inflammasome activation normally requires a two-step process, MoDC were initially incubated with lipopolysaccharide (LPS) in order to prime cells. Primed and unprimed cells were then stimulated with the aforementioned bacterial strains. We also assessed whether preincubation with the probiotic prior to ETEC infection modified the immune response via the inflammasome pathway. Phenotypical analysis by flow cytometry showed that monocytes and MoDC expressed the surface markers CD14, CD16, and CD1 continuously, whereas swine leucocyte antigen (SLA) II was upregulated during differentiation. Following LPS priming, NLRP3, interleukin (IL)-1β and IL-18 mRNA expression, and IL-1β protein release increased. In unprimed cells, ETEC upregulated the expression of inflammasome components at later time points than in LPS-primed MoDC. Preincubation with the probiotic did not influence NLRP3 inflammasome activation in comparison with cells infected with ETEC alone. We conclude that ETEC, but not E. faecium, was able to stimulate inflammasome components in porcine MoDC. The present experimental conditions revealed no NLRP3 inflammasome-dependent protective effects of E. faecium during a pathogenic ETEC challenge.