4.6 Article

Establishing Porcine Monocyte-Derived Macrophage and Dendritic Cell Systems for Studying the Interaction with PRRSV-1

Journal

FRONTIERS IN MICROBIOLOGY
Volume 7, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2016.00832

Keywords

PRRSV; macrophage; dendritic cell; CD163; CD169

Categories

Funding

  1. Animal and Plant Health Agency
  2. European Union [245141]
  3. Defra [SE0529]
  4. COST Action [FA902]
  5. BBSRC [BBS/E/I/00002035] Funding Source: UKRI
  6. Biotechnology and Biological Sciences Research Council [BBS/E/I/00002035] Funding Source: researchfish

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Monocyte-derived macrophages (MoMO) and monocyte-derived dendritic cells (MoDC) are two model systems well established in human and rodent systems that can be used to study the interaction of pathogens with host cells. Porcine reproductive and respiratory syndrome virus (PRRSV) is known to infect myeloid cells, such as macrophages (MO) and dendritic cells (DC). Therefore, this study aimed to establish systems for the differentiation and characterization of MoMO and MoDC for subsequent infection with PRRSV-1. M-CSF differentiated MoMO were stimulated with activators for classical (M1) or alternative (M2) activation. GM-CSF and IL-4 generated MoDC were activated with the well established maturation cocktail containing PAMPs and cytokines. In addition, MoMO and MoDC were treated with dexamethasone and IL-10, which are known immuno-suppressive reagents. Cells were characterized by morphology, phenotype, and function and porcine MO subsets highlighted some divergence from described human counterparts, while MoDC, appeared more similar to mouse and human DCs. The infection with PRRSV-1 strain Lena demonstrated different replication kinetics between MoMO and MoDC and within subsets of each cell type. While MoMO susceptibility was significantly increased by dexamethasone and IL-10 with an accompanying increase in CD163/CD169 expression, MoDC supported only a minimal replication of PRRSV These findings underline the high variability in the susceptibility of porcine myeloid cells toward PRRSV-1 infection.

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