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Open AccessArticle

Feline Infectious Peritonitis as a Systemic Inflammatory Disease: Contribution of Liver and Heart to the Pathogenesis

1
Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, 8057 Zurich, Switzerland
2
Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, 8057 Zurich, Switzerland
3
Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, ON N1G 2W1, Canada
4
Small Animal Hospital, Faculty of Veterinary Medicine, University of Helsinki, 00014 Helsinki, Finland
5
Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, University of Helsinki, 00014 Helsinki, Finland
6
Clinical Laboratory, Vetsuisse Faculty, University of Zurich, 8057 Zurich, Switzerland
7
Virology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, 3584 CL Utrecht, The Netherlands
*
Author to whom correspondence should be addressed.
Current addresses: The Royal (Dick) School of Veterinary Studies, Easter Bush Campus, University of Edinburgh, Edinburgh EH25 9RG, UK.
Current addresses: Cummings School of Veterinary Medicine, Tufts University, N. Grafton, MA 01536, USA.
Viruses 2019, 11(12), 1144; https://doi.org/10.3390/v11121144
Received: 31 October 2019 / Revised: 6 December 2019 / Accepted: 6 December 2019 / Published: 10 December 2019
(This article belongs to the Special Issue Feline Viruses and Viral Diseases)
Feline infectious peritonitis (FIP) is a fatal immune-mediated disease of cats, induced by feline coronavirus (FCoV). A combination of as yet poorly understood host and viral factors combine to cause a minority of FCoV-infected cats to develop FIP. Clinicopathological features include fever, vasculitis, and serositis, with or without effusions; all of which indicate a pro-inflammatory state with cytokine release. As a result, primary immune organs, as well as circulating leukocytes, have thus far been of most interest in previous studies to determine the likely sources of these cytokines. Results have suggested that these tissues alone may not be sufficient to induce the observed inflammation. The current study therefore focussed on the liver and heart, organs with a demonstrated ability to produce cytokines and therefore with huge potential to exacerbate inflammatory processes. The IL-12:IL-10 ratio, a marker of the immune system’s inflammatory balance, was skewed towards the pro-inflammatory IL-12 in the liver of cats with FIP. Both organs were found to upregulate mRNA expression of the inflammatory triad of cytokines IL-1β, IL-6, and TNF-α in FIP. This amplifying step may be one of the missing links in the pathogenesis of this enigmatic disease. View Full-Text
Keywords: feline infectious peritonitis; feline coronavirus; hepatocytes; cardiomyocytes; inflammatory cytokines; pathogenesis; systemic inflammatory response feline infectious peritonitis; feline coronavirus; hepatocytes; cardiomyocytes; inflammatory cytokines; pathogenesis; systemic inflammatory response
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MDPI and ACS Style

Malbon, A.J.; Fonfara, S.; Meli, M.L.; Hahn, S.; Egberink, H.; Kipar, A. Feline Infectious Peritonitis as a Systemic Inflammatory Disease: Contribution of Liver and Heart to the Pathogenesis. Viruses 2019, 11, 1144.

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