Characterization of the attachment and infection by Porcine reproductive and respiratory syndrome virus 1 isolates in bone marrow-derived dendritic cells

Li, Yanli; Darwich, Laila; Mateu, Enric

doi:10.1016/j.vetmic.2018.08.013

Cited by 4 publications

(4 citation statements)

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“…PRRSV1.1 isolate 3267 (Genbank accession n°JF276435) was used in the present study. This strain has been extensively used previously (23,(27)(28)(29)(30). Strain 3267 was propagated in AMs and used as a sixth passage (used in all experiments except otherwise indicated).…”

Section: Virus Production and Titrationmentioning

confidence: 99%

Interaction of Type 1 Porcine Reproductive and Respiratory Syndrome Virus With In Vitro Derived Conventional Dendritic Cells

Mateu

2021

Front. Immunol.

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The present study delineates the interaction of a typical PRRSV1.1 isolate 3267 (moderate virulence) with in vitro derived pig conventional dendritic cells, cDC1, cDC2, and a CD14+ population (designated as CD14+ DCs). cDC1 and cDC2 were not susceptible to 3267 infection, but a fraction of CD14+ DCs were infected. After exposure to the virus, all three DC types remained immature as determined by no increase of maturation molecules (MHC-I, MHC-II, CD80/86, CCR7), no release of cytokines, no modification of antigen presentation abilities, and no alteration of endocytic/phagocytic capabilities. However, when infected MARC-145 cells were used as a source of viral antigens, cDC2 and CD14+ DCs showed a significant increase in the expression of maturation molecules and substantial release of cytokines, notably IL-12/IL-23p40 (by both DC types) and IL-10 (by CD14+ DCs). To address the impact of PRRSV1 3267 on TLR3- and TLR7-mediated activation, cDC1, cDC2, and CD14+ DCs were inoculated by the virus (live or UV-inactivated) for 6 h prior to or simultaneously with the addition of poly I:C (TLR3 ligand) or gardiquimod (TLR7 ligand; not used for cDC1). Compared with using TLR ligand alone, combination with the virus did not result in any alteration to the maturation markers on all DC types but changed the cytokine response to either TLR3 or TLR7 ligand. Pre-exposure of cDC2 or CD14+ DCs to the live virus resulted in an increased production of IFN-α upon poly I:C stimulation, while pre-exposure to UV-inactivated virus tended to enhance the release of IL-10 upon gardiquimod stimulation. Simultaneous addition of the live virus and the TLR ligand either had no effect (mainly in cDC2) or impaired most of the cytokine release after gardiquimod stimulation (in CD14+ DCs). When used as antigen presenting cells, cDC2 pre-inoculated by the live virus before addition of gardiquimod impaired the proliferation of CD4–CD8– T cells. In the case of CD14+ DCs, pre-exposure to the live virus or simultaneously added with TLR3 or TLR7 ligand largely decreased the proliferation of CD4–CD8+ and CD4–CD8+ T-cell subsets. For cDC1, no significant changes were observed in cytokine responses or T-cell proliferation after poly I:C stimulation. Of note, cDC1 had a short life during in vitro culturing, for which the results obtained might be biased. Overall, exposure to PRRSV1 did not induce maturation of cDC1, cDC2, or CD14+ DCs, but modified TLR3 and TLR7-associated responses (except for cDC1), which may affect the development of adaptive immunity during PRRSV1 infection. Moreover, the sensing of infected cells was different from that of the free virus.

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Section: Virus Production and Titrationmentioning

confidence: 99%

Interaction of Type 1 Porcine Reproductive and Respiratory Syndrome Virus With In Vitro Derived Conventional Dendritic Cells

Mateu

2021

Front. Immunol.

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“…Frydas et al [11] also observed Lena strain infection in CD163 − Sn − cells in the nasal mucosa explants and Doeschl-Wilson et al [45] found that the population of infected CD163 − PAM increased over incubation time. Also, Li et al [46] recently demonstrated PRRSV infection in CD163 − , CD163 lo and CD163 hi cells. This means that in vitro, CD163 positive cells may still be infected with certain PRRSV strains.…”

Section: Discussionmentioning

confidence: 94%

Isolation and characterization of a new population of nasal surface macrophages and their susceptibility to PRRSV-1 subtype 1 (LV) and subtype 3 (Lena)

Xie

Vanderheijden

et al. 2020

Vet Res

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Sialoadhesin (Sn) and CD163 have been recognized as two important mediators for porcine reproductive and respiratory syndrome virus (PRRSV) in host macrophages. Recently, it has been demonstrated that the highly virulent Lena strain has a wider macrophage tropism than the low virulent LV strain in the nasal mucosa. Not only CD163 + Sn + macrophages are infected by Lena but also CD163 + Sn − macrophages. This suggests that an alternative receptor exists for binding and internalization of PRRSV Lena in the CD163 + Sn − macrophages. Further investigation to find the new entry receptor was hampered by the difficulty of isolating these macrophages from the nasal mucosa. In the present study, a new population of CD163 + Sn − cells has been identified that is specifically localized in the nasal lamina propria and can be isolated by an intranasal digestion approach. Isolated nasal cells were characterized using specific cell markers and their susceptibility to two different PRRSV-1 strains (LV and Lena) was tested. Upon digestion, 3.2% (flow cytometry)-6.4% (confocal microscopy) of the nasal cells were identified as CD163 + and all (99.7%) of these CD163 + cells were Sn −. These CD163 + Sn − cells, designated as "nasal surface macrophages", showed a 4.9 times higher susceptibility to the Lena strain than to the LV strain. Furthermore, the Lena-inoculated cell cultures showed an upregulation of CD163. These results showed that our new cell isolation system is ideal for the further functional and phenotypical analysis of the new population of nasal surface macrophages and further research on the molecular pathogenesis of PRRSV in the nose.

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“…A most recent publication from Mateu’s group had characterized, in more detail, the interaction between PRRSV-1 strains and BMDC [76] when PRRSV-1 replication and attachment in immature (iBMDC) and mature BMDC (mBMDC) was studied. Replication kinetics showed that titres in iBMDC were significantly higher than mBMDC by 24 hpi and iBMDC were more efficient in the support of PRRSV-1 replication than mBMDC.…”

Section: Innate Cellular Immune Responses Triggered By Prrsvmentioning

confidence: 99%

“…iBMDC attachment by all of the strain was possible in cells that lack porcine CD163 or sialoadhesin (CD169) receptors or in cells with heparan sulfate (unspecific attachment receptor) removed. PRRSV-1 nucleocapsid could be observed in CD163− iBMDC and those cells were only infected when CD163low/hi cells were present, indicating that the susceptibility of CD163− cells derived as result of the milieu that was created by CD163+ infected BMDC, by receptor-independent mechanisms or that some cells expressed CD163 at levels that were below the technical sensitivity [76].…”

Section: Innate Cellular Immune Responses Triggered By Prrsvmentioning

confidence: 99%

Cellular Innate Immunity against PRRSV and Swine Influenza Viruses

Crisci

Fraile

Montoya

2019

Veterinary Sciences

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Porcine respiratory disease complex (PRDC) is a polymicrobial syndrome that results from a combination of infectious agents, such as environmental stressors, population size, management strategies, age, and genetics. PRDC results in reduced performance as well as increased mortality rates and production costs in the pig industry worldwide. This review focuses on the interactions of two enveloped RNA viruses—porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza virus (SwIV)—as major etiological agents that contribute to PRDC within the porcine cellular innate immunity during infection. The innate immune system of the porcine lung includes alveolar and parenchymal/interstitial macrophages, neutrophils (PMN), conventional dendritic cells (DC) and plasmacytoid DC, natural killer cells, and γδ T cells, thus the in vitro and in vivo interactions between those cells and PRRSV and SwIV are reviewed. Likewise, the few studies regarding PRRSV-SwIV co-infection are illustrated together with the different modulation mechanisms that are induced by the two viruses. Alterations in responses by natural killer (NK), PMN, or γδ T cells have not received much attention within the scientific community as their counterpart antigen-presenting cells and there are numerous gaps in the knowledge regarding the role of those cells in both infections. This review will help in paving the way for future directions in PRRSV and SwIV research and enhancing the understanding of the innate mechanisms that are involved during infection with these viruses.

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Characterization of the attachment and infection by Porcine reproductive and respiratory syndrome virus 1 isolates in bone marrow-derived dendritic cells

Cited by 4 publications

References 50 publications

Interaction of Type 1 Porcine Reproductive and Respiratory Syndrome Virus With In Vitro Derived Conventional Dendritic Cells

Interaction of Type 1 Porcine Reproductive and Respiratory Syndrome Virus With In Vitro Derived Conventional Dendritic Cells

Isolation and characterization of a new population of nasal surface macrophages and their susceptibility to PRRSV-1 subtype 1 (LV) and subtype 3 (Lena)

Cellular Innate Immunity against PRRSV and Swine Influenza Viruses

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