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In vivo cytokine response to experimental feline infectious peritonitis virus infection
Feline infectious peritonitis virus (FIPV) is a coronavirus that causes sporadic fatal disease in cats characterized by vasculitis, granulomatous inflammation and effusive pleuritis/peritonitis. Histologic changes in lymphoid tissues include lymphoid hyperplasia, lymphoid depletion, histiocytosis, a...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier B.V.
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7117329/ https://www.ncbi.nlm.nih.gov/pubmed/14637034 http://dx.doi.org/10.1016/j.vetmic.2003.08.010 |
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author | Dean, Gregg A. Olivry, Thierry Stanton, Christine Pedersen, Niels C. |
author_facet | Dean, Gregg A. Olivry, Thierry Stanton, Christine Pedersen, Niels C. |
author_sort | Dean, Gregg A. |
collection | PubMed |
description | Feline infectious peritonitis virus (FIPV) is a coronavirus that causes sporadic fatal disease in cats characterized by vasculitis, granulomatous inflammation and effusive pleuritis/peritonitis. Histologic changes in lymphoid tissues include lymphoid hyperplasia, lymphoid depletion, histiocytosis, and granuloma formation. Although viremia occurs, histologic lesions are not found uniformly throughout lymphoid tissues. We used experimental infection of cats with a highly pathogenic FIPV isolate, UCD8, to study histologic lesions, virus replication, and cytokine expression in multiple lymphoid tissues during the effusive phase of disease. Viral RNA was found in 76% of central tissues (mediastinal lymph node, spleen, mesenteric lymph node) examined, as compared to 27% of peripheral tissues (popliteal lymph node, cervical lymph node, femoral bone marrow). All tissues positive for virus replication also demonstrated lymphoid depletion. Generally, affected tissues had lower levels of IL-4 and IL-12–p40 mRNA and higher levels of IL-10 mRNA. Although no differences in IFN-γ or TNF-α mRNA were measured, TNF-α protein expression was greater in affected tissues and demonstrated a shift in the source of TNF-α from macrophages to lymphocytes. Together, these results colocalize FIPV replication, lymphocyte depletion in tissues, and alterations in cytokine transcription and translation. A possible role for TNF-α in the previously described FIPV-induced lymphocyte apoptosis is also suggested. |
format | Online Article Text |
id | pubmed-7117329 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | Elsevier B.V. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71173292020-04-02 In vivo cytokine response to experimental feline infectious peritonitis virus infection Dean, Gregg A. Olivry, Thierry Stanton, Christine Pedersen, Niels C. Vet Microbiol Article Feline infectious peritonitis virus (FIPV) is a coronavirus that causes sporadic fatal disease in cats characterized by vasculitis, granulomatous inflammation and effusive pleuritis/peritonitis. Histologic changes in lymphoid tissues include lymphoid hyperplasia, lymphoid depletion, histiocytosis, and granuloma formation. Although viremia occurs, histologic lesions are not found uniformly throughout lymphoid tissues. We used experimental infection of cats with a highly pathogenic FIPV isolate, UCD8, to study histologic lesions, virus replication, and cytokine expression in multiple lymphoid tissues during the effusive phase of disease. Viral RNA was found in 76% of central tissues (mediastinal lymph node, spleen, mesenteric lymph node) examined, as compared to 27% of peripheral tissues (popliteal lymph node, cervical lymph node, femoral bone marrow). All tissues positive for virus replication also demonstrated lymphoid depletion. Generally, affected tissues had lower levels of IL-4 and IL-12–p40 mRNA and higher levels of IL-10 mRNA. Although no differences in IFN-γ or TNF-α mRNA were measured, TNF-α protein expression was greater in affected tissues and demonstrated a shift in the source of TNF-α from macrophages to lymphocytes. Together, these results colocalize FIPV replication, lymphocyte depletion in tissues, and alterations in cytokine transcription and translation. A possible role for TNF-α in the previously described FIPV-induced lymphocyte apoptosis is also suggested. Elsevier B.V. 2003-12-02 2003-11-18 /pmc/articles/PMC7117329/ /pubmed/14637034 http://dx.doi.org/10.1016/j.vetmic.2003.08.010 Text en Copyright © 2003 Elsevier B.V. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Dean, Gregg A. Olivry, Thierry Stanton, Christine Pedersen, Niels C. In vivo cytokine response to experimental feline infectious peritonitis virus infection |
title | In vivo cytokine response to experimental feline infectious peritonitis virus infection |
title_full | In vivo cytokine response to experimental feline infectious peritonitis virus infection |
title_fullStr | In vivo cytokine response to experimental feline infectious peritonitis virus infection |
title_full_unstemmed | In vivo cytokine response to experimental feline infectious peritonitis virus infection |
title_short | In vivo cytokine response to experimental feline infectious peritonitis virus infection |
title_sort | in vivo cytokine response to experimental feline infectious peritonitis virus infection |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7117329/ https://www.ncbi.nlm.nih.gov/pubmed/14637034 http://dx.doi.org/10.1016/j.vetmic.2003.08.010 |
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