CCL2 and CCL5 driven attraction of CD172a+ monocytic cells during an equine herpesvirus type 1 (EHV-1) infection in equine nasal mucosa and the impact of two migration inhibitors, rosiglitazone (RSG) and quinacrine (QC).
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Equine herpesvirus type 1 (EHV-1) causes respiratory disease, abortion and neurological disorders in horses. Besides epithelial cells, CD172a + monocytic cells become infected with EHV-1 in the respiratory mucosa and transport the virus from the apical side of the epithelium to the lamina propria en route to the lymph and blood circulation. Whether CD172a + monocytic cells are specifically recruited to the infection sites in order to pick up virus is unknown. In our study, equine nasal mucosa explants were inoculated with EHV-1 neurological strains 03P37 and 95P105 or the non-neurological strains 97P70 and 94P247 and the migration of monocytic cells was examined by immunofluorescence. Further, the role of monokines CCL2 and CCL5 was determined and the effect of migration inhibitors rosiglitazone (RSG) or quinacrine was analyzed. It was shown that with neurological strains but not with the non-neurological strains, CD172a + cells specifically migrated towards EHV-1 infected regions and that CCL2 and CCL5 were involved. CCL2 started to be expressed in infected epithelial cells at 24 h post-incubation (hpi) and CCL5 at 48 hpi, which corresponded with the CD172a + migration. RSG treatment of EHV-1-inoculated equine nasal mucosa had no effect on the virus replication in the epithelium, but decreased the migration of CD172a + cells in the lamina propria. Overall, these findings bring new insights in the early pathogenesis of EHV-1 infections, illustrate differences between neurological and non-neurological strains and show the way for EHV-1 treatment.
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In nasal mucosal explants, EHV-1 elicited the production of chemokines CCL2 and CCL5 already at 24 hours post-inoculation in order to attract target CD172a+ cells.
“In nasal mucosal explants, EHV-1 elicited the production of chemokines (e.g., CCL2 and CCL5), already at 24 hpi, in order to attract target CD172a+ cells (Gryspeerdt et al., 2010; Zhao et al., 2017).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Zhao et al., 2017
The Discussion (page unavailable) says CCL2 and CCL5 were first detected at 24 hpi and were involved in attracting CD172a+ cells. However, the Results and Discussion limit the increased chemokine production and cell migration to neurological EHV-1 strains; non-neurological strains did not show a significant increase. The Results also report a significant CCL5 increase only from 48 hpi. (LLM, conf=0.87)
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References 43 · Cited by 23
- Authors
- Zhao, J., Poelaert, K. C. K., Van Cleemput, J., & Nauwynck, H. J.
- Affiliations
- Ghent University (BE)
- Corresponding author
- Nauwynck, Hans J.
- Venue
- Veterinary Research
- Published
- 2017-02-27
- Volume
- 48
- Issue
- 1
- Pages
- 14-14
- ISSN
- 0928-4249 (ISSN-L)
- 1297-9716
- PMC
- PMC5327560
- OpenAlex
- W2590648030
- Cited by
- 23
- References
- 43
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 6 · 2020: 3 · 2019: 3 · 2018: 1
- FWCI
- 1.50
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Veterinary Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion, cc-by)
- HAL (submittedVersion, other-oa)
- Funders
- China Scholarship Council (201203250001)
- Institute for the promotion of Innovation through Science and Technology in Flanders (IWT-Vlaanderen) (141627)
- Research Foundation Flanders (FWO) (11Y5415N)
- Topics
- Health Sciences › Medicine › Epidemiology › Herpesvirus Infections and Treatments
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Animal Virus Infections Studies
- Keywords
- equine herpesvirus 1, MCP-1, RANTES, chemokines, cell migration, rosiglitazone, quinacrine, nasal mucosa, viral pathogenesis, horses, lamina propria
- MeSH terms
- Rosiglitazone, Animals, Cell Movement, Herpesvirus 1, Equid, Fluorescent Antibody Technique, Herpesviridae Infections, Horse Diseases, Horses, Monocytes, Nasal Mucosa, Quinacrine, Receptors, Immunologic, Chemokine CCL2, Chemokine CCL5, Thiazolidinediones
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