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Interaction of the European genotype porcine reproductive and respiratory syndrome virus (PRRSV) with sialoadhesin (CD169/Siglec-1) inhibits alveolar macrophage phagocytosis

Miet De Baere UGent, Hanne Van Gorp UGent, Peter Delputte UGent and Hans Nauwynck UGent (2012) VETERINARY RESEARCH. 43.
abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is an arterivirus that shows a restricted in vivo tropism for subsets of porcine macrophages, with alveolar macrophages being major target cells. The virus is associated with respiratory problems in pigs of all ages and is commonly isolated on farms with porcine respiratory disease complex (PRDC). Due to virus-induced macrophage death early in infection, PRRSV hampers the innate defence against pathogens in the lungs. In addition, the virus might also directly affect the antimicrobial functions of macrophages. This study examined whether interaction of European genotype PRRSV with primary alveolar macrophages (PAM) affects their phagocytic capacity. Inoculation of macrophages with both subtype I PRRSV (LV) and subtype III PRRSV (Lena) showed that the virus inhibits PAM phagocytosis. Similar results were obtained using inactivated PRRSV (LV), showing that initial interaction of the virion with the cell is sufficient to reduce phagocytosis, and that no productive infection is required. When macrophages were incubated with sialoadhesin- (Sn) or CD163-specific antibodies, two entry mediators of the virus, only Sn-specific antibodies downregulated the phagocytic capacity of PAM, indicating that interaction with Sn, but not CD163, mediates the inhibitory effect of PRRSV on phagocytosis. In conclusion, this study shows that European genotype PRRSV inhibits PAM phagocytosis in vitro, through the interaction with its internalization receptor Sn. If similar events occur in vivo, this interaction may be important in the development of PRDC, as often seen in the field.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
CYTOKINE PRODUCTION, IN-VITRO, PSEUDORABIES VIRUS, INFECTION, PIGS, LUNGS, APOPTOSIS, ISOLATE, EXPRESSION, ANTIBODIES
journal title
VETERINARY RESEARCH
Vet. Res.
volume
43
article_number
47
pages
10 pages
Web of Science type
Article
Web of Science id
000306646000001
JCR category
VETERINARY SCIENCES
JCR impact factor
3.426 (2012)
JCR rank
1/142 (2012)
JCR quartile
1 (2012)
ISSN
0928-4249
DOI
10.1186/1297-9716-43-47
language
English
UGent publication?
yes
classification
A1
copyright statement
I have retained and own the full copyright for this publication
id
2942476
handle
http://hdl.handle.net/1854/LU-2942476
date created
2012-06-29 09:27:14
date last changed
2012-09-11 11:22:27
@article{2942476,
  abstract     = {Porcine reproductive and respiratory syndrome virus (PRRSV) is an arterivirus that shows a restricted in vivo tropism for subsets of porcine macrophages, with alveolar macrophages being major target cells. The virus is associated with respiratory problems in pigs of all ages and is commonly isolated on farms with porcine respiratory disease complex (PRDC). Due to virus-induced macrophage death early in infection, PRRSV hampers the innate defence against pathogens in the lungs. In addition, the virus might also directly affect the antimicrobial functions of macrophages. This study examined whether interaction of European genotype PRRSV with primary alveolar macrophages (PAM) affects their phagocytic capacity. Inoculation of macrophages with both subtype I PRRSV (LV) and subtype III PRRSV (Lena) showed that the virus inhibits PAM phagocytosis. Similar results were obtained using inactivated PRRSV (LV), showing that initial interaction of the virion with the cell is sufficient to reduce phagocytosis, and that no productive infection is required. When macrophages were incubated with sialoadhesin- (Sn) or CD163-specific antibodies, two entry mediators of the virus, only Sn-specific antibodies downregulated the phagocytic capacity of PAM, indicating that interaction with Sn, but not CD163, mediates the inhibitory effect of PRRSV on phagocytosis. In conclusion, this study shows that European genotype PRRSV inhibits PAM phagocytosis in vitro, through the interaction with its internalization receptor Sn. If similar events occur in vivo, this interaction may be important in the development of PRDC, as often seen in the field.},
  articleno    = {47},
  author       = {De Baere, Miet and Van Gorp, Hanne and Delputte, Peter and Nauwynck, Hans},
  issn         = {0928-4249},
  journal      = {VETERINARY RESEARCH},
  keyword      = {CYTOKINE PRODUCTION,IN-VITRO,PSEUDORABIES VIRUS,INFECTION,PIGS,LUNGS,APOPTOSIS,ISOLATE,EXPRESSION,ANTIBODIES},
  language     = {eng},
  pages        = {10},
  title        = {Interaction of the European genotype porcine reproductive and respiratory syndrome virus (PRRSV) with sialoadhesin (CD169/Siglec-1) inhibits alveolar macrophage phagocytosis},
  url          = {http://dx.doi.org/10.1186/1297-9716-43-47},
  volume       = {43},
  year         = {2012},
}

Chicago
De Baere, Miet, Hanne Van Gorp, Peter Delputte, and Hans Nauwynck. 2012. “Interaction of the European Genotype Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) with Sialoadhesin (CD169/Siglec-1) Inhibits Alveolar Macrophage Phagocytosis.” Veterinary Research 43.
APA
De Baere, M., Van Gorp, H., Delputte, P., & Nauwynck, H. (2012). Interaction of the European genotype porcine reproductive and respiratory syndrome virus (PRRSV) with sialoadhesin (CD169/Siglec-1) inhibits alveolar macrophage phagocytosis. VETERINARY RESEARCH, 43.
Vancouver
1.
De Baere M, Van Gorp H, Delputte P, Nauwynck H. Interaction of the European genotype porcine reproductive and respiratory syndrome virus (PRRSV) with sialoadhesin (CD169/Siglec-1) inhibits alveolar macrophage phagocytosis. VETERINARY RESEARCH. 2012;43.
MLA
De Baere, Miet, Hanne Van Gorp, Peter Delputte, et al. “Interaction of the European Genotype Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) with Sialoadhesin (CD169/Siglec-1) Inhibits Alveolar Macrophage Phagocytosis.” VETERINARY RESEARCH 43 (2012): n. pag. Print.